Transvenous Cardiac Pacing 

Updated: Mar 06, 2018
Author: Ali A Sovari, MD, FACP, FACC; Chief Editor: Vincent Lopez Rowe, MD 

Overview

Background

This article describes transvenous cardiac pacing. In a healthy heart, electrical impulses are generated in the sinoatrial (SA) node (sinus node), which is near the junction of the superior vena cava (SVC) and the right atrium (RA). The specialized cells of the SA node generate electrical impulses faster than other parts of the conduction system and with automaticity; therefore, these cells are usually the dominant natural pacemakers of the heart. The impulse is then conducted through the RA and left atrium (LA) and reaches the atrioventricular (AV) node.

The AV junction, which is at the base of the interatrial septum and extends into the interventricular septum, has two main parts: the AV node in the upper part, and the bundle of His in the lower part. In a healthy heart, the AV node is the only electrical connection between the atria and the ventricles. The inherent delay in transmitting the electrical impulse from the atria to the ventricles provides the appropriate diastolic duration to enable ventricular filling.

The His bundle divides into the left and right bundle branches and then into the Purkinje fibers, which conduct the impulse rapidly through the ventricles to produce rapid and simultaneous ventricular contractions. In general, symptomatic abnormalities of the conduction system are the main indications for cardiac pacing, a method by which a small pulsed electrical current is artificially delivered to the heart.

Of the several methods for temporary pacing of the heart (transcutaneous, transvenous, transesophageal, transthoracic, and epicardial), transvenous and transcutaneous cardiac pacing are the most commonly used. The main factor that dictates the use of one approach instead of another is the urgency of the need for pacing.

In an emergency where a patient is experiencing cardiac symptoms or asystole, transcutaneous pacing is the method of choice. Nevertheless, transvenous pacing has the following advantages over the transcutaneous method:

  • Enhanced patient comfort
  • Greater reliability
  • Ability to pace the atrium

However, because transvenous pacing requires central venous access, it cannot be initiated as fast as transcutaneous pacing can, and it is associated with several complications that result from obtaining venous access.

A common scenario is one in which transcutaneous pacing is employed first in an emergency, followed by transvenous placement of a lead that will enable a longer period of pacing and evaluation in patients who may require permanent pacing later during their hospitalization.

Indications

Transvenous cardiac pacing can be used as a bridge to permanent pacing when permanent pacing is not available, when the pacing need is only temporary, or when further evaluation is required.[1] Therefore, all indications for permanent cardiac pacing are indications for transvenous pacing as well. Temporary pacing is appropriate when a permanent pacemaker must be replaced, repaired, or changed or when permanent pacing fails. In emergencies (eg, asystole), transcutaneous pacing may be the most appropriate type of temporary pacing.

Recommended indications for cardiac pacing can be complex and depend on a combination of presenting symptoms and electrocardiographic (ECG) findings. These recommendations, along with their level of supporting evidence, are well summarized by the American College of Cardiology (ACC) and the American Heart Association (AHA).[2, 3]

Because transvenous pacing is a temporary method, it may be indicated for treating a reversible condition for which permanent pacing is contraindicated. For example, Ho et al reported using transcutaneous pacing in patients with bradycardia due to hypothermia.[4]

Temporary cardiac pacing is occasionally used to determine whether a patient requires permanent pacing. However, patients treated with cardiac pacing may become pacemaker-dependent and exhibit asystole when pacing is terminated, even though they may not have experienced asystole in the absence of pacing.

Although temporary transvenous cardiac pacing is indicated primarily for the treatment of bradycardia and various types of heart block, intermittent overdrive pacing can also be used as an antitachycardic treatment for a variety of atrial and ventricular tachycardias, such as postoperative atrial flutter or monomorphic ventricular tachycardia (VT). Pacing is also used to prevent bradycardia-dependent tachycardias, such as torsades de pointes.

Reversible causes of heart block that may call for temporary cardiac pacing include the following:

  • Injury to the SA node or other parts of the conduction system after cardiac surgery (injuries that occur after coronary bypass surgery tend to be temporary, but those sustained after valve surgery or cardiac transplant may not be reversible)
  • Chest and cardiac trauma associated with either temporary SA node or AV node dysfunction
  • Metabolic and electrolyte derangements (eg, hyperkalemia)
  • Drug-induced bradyarrhythmia (eg, digitalis toxicity); if treatment with the drug must be continued and there is no alternative, permanent pacing should be considered
  • Other diseases (eg, Lyme disease, bacterial endocarditis) that may be associated with temporary damage to the SA node or the AV node

Contraindications

In general, temporary cardiac pacing should not be considered for asymptomatic patients who have a fairly stable rhythm (eg, a first-degree AV block or a Mobitz I or stable escape rhythm). For example, pacing an asymptomatic patient with a stable escape rhythm may render that individual dependent on pacing, and withholding pacing may then cause asystole.

Although the aforementioned rhythms are stable for the most part, there are exceptions (eg, a Mobitz I rhythm with a wide QRS may originate from an infra-AV nodal area and therefore may progress to complete heart block). When in doubt, having transcutaneous pacing ready for use in emergencies may be reasonable.

Technical Considerations

In 1974, the ACC and the AHA proposed a three-digit code system for categorizing the basic functions of pacemakers. The North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) continued to expand these codes, and the coding system was subsequently updated in 2002. Currently, pacemaker function is described by means of the following position codes, which are generic and are used for all brands of pacemakers:

  • Position I - This position indicates the chamber or chambers paced, with A standing for “atrium,” V for “ventricle,” and D for “dual-chamber” (meaning that both the RA and the right ventricle [RV] can be paced)
  • Position II - The same letters listed above are used refer to the chamber or chambers sensed, with S standing for “single-chamber” (meaning that the pacemaker can pace only one chamber) and O indicating that the pacemaker lacks sensing capability (it may be used in asynchronous pacing)
  • Position III - This position indicates how the pacemaker responds to a sensed event, with I indicating that the sensed event inhibits the pacemaker output, T that the sensed event triggers the output, and D that both capabilities are available; dual response is possible only in a dual-chamber pacemaker—for example, a sensed event in the atrium can inhibit the output in the atrium and trigger the output in the ventricle, and in such cases, ventricular output usually occurs with a delay to mimic the normal PR interval and may be inhibited if the atrial pulse is conducted normally through the AV node
  • Position IV - This position indicates programmability and rate modulation capability, with R indicating that the rate can be changed, depending on whether the patient is active, and O, which may not be explicitly mentioned (ie, DDD is understood to be equivalent to DDDO), indicating that rate modulation is not available or is not used
  • Position V - This position refers to multisite pacing, with A indicating that the pacemaker can pace multiple sites in one or both atria, V that it can pace multiple sites in one or both ventricles, D that it can pace multiple sites in both the atria and the ventricles, and O that the multisite capability is not available or is not used

These position codes are used to describe pacemaker modes, as follows:

  • VVI mode - The device paces and senses the RV, and a sensed event in the ventricle inhibits the pacemaker from pacing or producing any output
  • AAI mode - The pacemaker paces and senses the atrium, and the sensing of an event (eg, sensing atrial activity within 1 second) inhibits the pacemaker from pacing
  • DDD mode - The pacemaker paces both the atria and the ventricles; it can sense both chambers, and the response can be both triggering or inhibitory
  • DDDR mode - The pacemaker has all the capabilities of the VVI, AAI, and DDD modes, as well as rate modulation capability
 

Periprocedural Care

Equipment

To obtain venous access, a central venous access kit, a temporary external transvenous pacing generator (single-chamber or dual-chamber), and a pacing lead are required, along with the following:

  • Sterile gown, gloves, cap, and face shield
  • Either a drape or towels for skin preparation
  • Lidocaine
  • Sterile gauze
  • Syringes
  • Scalpel
  • Saline flush
  • Catheter
  • Dilator
  • Needle
  • Wire
  • Suture
  • Needle driver

Fluoroscopy, electrocardiography (ECG), or echocardiography is required to direct intracardiac lead placement. Fluoroscopy is the modality most commonly used for this purpose and is the best direct visual aid for placement of the pacing lead within the heart. If fluoroscopy is not available, ECG or echocardiography may be used instead. An external defibrillator should also be available during the procedure.

Pacing leads

The standard pacing leads are bipolar leads that are usually 3-6 French in diameter. (Multipolar leads with more electrodes are being studied.[5] ) Some catheters have an inflatable balloon between the electrodes (floating catheters; see the first and second images below); others are semirigid (semifloating catheters; see the third and fourth images below).

Floating catheter that follows circulation flow. I Floating catheter that follows circulation flow. It may be used when fluoroscopy is not available.
Tip of floating catheter that inflates with 1-1.5 Tip of floating catheter that inflates with 1-1.5 mL of air.
Semirigid catheter typically used when fluoroscopy Semirigid catheter typically used when fluoroscopy is available for implantation.
Tip of semirigid catheter. Tip of semirigid catheter.

Semifloating catheters respond better to manipulation, but floating catheters are more useful when fluoroscopy is not available for placement of the lead. A floating catheter follows the flow to reach the right ventricle (RV). When it reaches the RV, it is deflated to prevent it from entering the right pulmonary artery. Single-pass atrioventricular (AV) sequential pacing catheters have proximal electrodes for atrial pacing and distal electrodes for ventricular pacing.

In addition, preformed atrial J-shaped catheters provide more stability for atrial pacing. Pacing is also made possible by using the proximal port or the distal port of a pulmonary artery catheter to pass a J-shaped atrial pacing wire or a ventricular pacing wire, respectively. In most situations, single-chamber RV pacing is the preferred choice. Temporary pacing leads do not have an active fixation mechanism.

External generators

External generators come in either single-chamber or dual-chamber models (see the images below). A single-chamber generator can usually modify rate (up to 180 beats/min), output (up to 20 mA), and sensitivity. An external dual-chamber pacing generator has most of the features necessary for dual-chamber pacing, along with antitachycardia pacing features.

External single-chamber pacing unit that has 3 mai External single-chamber pacing unit that has 3 main features to control rate, current, and sensitivity.
External pacemaker unit capable of complex dual-ch External pacemaker unit capable of complex dual-chamber pacing.
 

Technique

Transvenous Pacing

In nonemergency situations, the first step is to explain the procedure to the patient and obtain his or her baseline rate, rhythm, and vital signs. All equipment needed for the procedure should be ready. Insertion of the pacing lead is then carried out as follows.

Venous access

The first step in transvenous pacing is obtaining venous access. Before venous access is obtained, the subcutaneous tissue and area around the course of the needle should be anesthetized with lidocaine 1% or 2%, with or without epinephrine.

The internal jugular vein and the subclavian vein are the most common sites of venous access for temporary transvenous pacing. Although a peripheral venous site may facilitate control of bleeding complications caused by the procedure, such sites are not frequently used, because of the circuitous course the lead must take, the increased chance of thrombosis and infection, and the greater risk of complications associated with limb movement.

Access via the internal jugular vein gives the pacing lead a straight route to the right atrium (RA), reserves the subclavian vein for possible future permanent pacemaker implantation, and is associated with fewer incidences of pneumothorax and hemothorax. For further reading on obtaining venous access, please see the following:

Placement of pacing lead

When fluoroscopy is available, a semirigid pacing lead may be used. The lead is advanced until it reaches the RA. The desirable location for pacing the right ventricle (RV) is usually the apex. To reach the RV, the catheter is passed through the tricuspid valve; this may be accomplished more easily if the clinician forms a loop in the atrium and rotates the catheter. Once in the RV, the catheter is advanced gradually toward the apex and septum. Some clinicians may prefer RV outflow tract positioning for more stability.[6]

The most desirable atrial pacing location is the right atrial appendage. A preformed J-shaped catheter can be advanced anteriorly and medially in the low RA to reach the right atrial appendage. It is then withdrawn to the superior vena cava (SVC) while being rotated anteriorly to permit advancement into the right atrial appendage.

When fluoroscopy is not available, electrocardiography (ECG) may be used to guide lead placement. In such cases, it is better to use a balloon-tipped catheter. When the balloon-tipped catheter is inflated after being inserted into the vein, it will follow the flow, and the distal electrodes of the catheter can be connected to the V1 lead of the ECG device to record a unipolar electrocardiogram.

Alternatively, the distal electrode can be connected to the right arm lead and the proximal electrode to the left arm lead to record a bipolar lead I electrocardiogram. In the inferior vena cava (IVC) and the SVC, ECG shows a small wave of atrial activity (the so-called A wave) and a large wave of ventricular activity (the so-called V wave), as does a normal surface ECG.

When the catheter enters the RA, the A wave becomes larger than the V wave because the catheter records nearby atrial activity much better than it does distant ventricular activity. When the catheter passes the tricuspid valve and enters the RV, the relative amplitudes of the A and V waves reverse, so that the A wave becomes smaller than the V wave. When the catheter is in contact with the RV wall, the V wave is very large (>6 mV) and produces ST-segment elevation as an indication of injury current.

In emergencies (eg, asystole), transcutaneous pacing should be tried first. If transvenous pacing is tried, the catheter should be advanced during asynchronous pacing at maximum output until the ventricle has been captured and a palpable pulse is detected in the patient.

Echocardiography may also be used to guide lead placement and appears to be feasible and safe in this application,[7] but it is less commonly employed.

When the lead is in place, it is connected to the external generator, and the appropriate mode is selected. The capture and sensing thresholds are also tested. In an emergency, the highest output should be tried first; it should then be gradually reduced until the capture is lost.

If the situation is not an emergency, the rate is set 10-20 beats/min above the intrinsic heart rate, and the output is initially set very low and then gradually increased until capture occurs. The output should be set to a value at least two to three times higher than the threshold to ensure a safe margin for any change that occurs in the capture threshold, which is usually less than 1 mA. A slightly higher capture threshold is acceptable for atrial leads because they are less stable than ventricular leads.

To check the sensing threshold (if it is needed in the demand pacing mode), the pacing rate should be set lower than the intrinsic heart rate. The value of the sensing threshold should then be gradually increased until the pacemaker fails to sense the intrinsic activity and consequently begins firing. The sensing threshold is usually more than 5 mV in the ventricle and is much lower in the atrium. The AV interval in AV sequential pacing is usually between 100 and 200 ms, which is comparable to a normal PR interval.

Confirmation of pacing lead position

Once the lead has been placed, its location should be confirmed by means of ECG and chest radiography. On ECG, a paced QRS should exhibit left bundle-branch block (LBBB) morphology because the lead is located in the RV.

The axis of the paced QRS may provide additional useful information. The axis may be determined by checking leads I and aVF. A positive deflection in lead I indicates a leftward axis, and a negative deflection in that lead indicates a rightward axis. A positive QRS deflection in lead aVF indicates an inferior axis, and a negative QRS deflection in that lead indicates a superior axis.

Accordingly, proper RV lead placement in the apex should be associated with LBBB morphology and a superior axis in the paced QRS complexes. If the pacing lead is in the RV outflow tract, the paced QRS complexes show LBBB morphology and an inferior axis (which might also be rightward). Thus, on a surface ECG, lead V1 shows mainly a positive QRS deflection and lead aVF a positive QRS deflection; lead I may show a negative QRS deflection. A pacing lead in the coronary sinus will show right bundle-branch block (RBBB) morphology.

Unless RV outflow tract and left ventricular (LV) pacing are planned, the aforementioned ECG characteristics are evidence of malpositioning, even if the malpositioning is not detected on chest radiography. On an anteroposterior chest radiograph, the tip of a catheter in the RV should be pointed slightly inferiorly and should be near the lateral border of the heart. On a lateral view, it should point anteriorly a few centimeters behind the sternum. A J-shaped atrial pacing lead should point cranially to the left and slightly anteriorly.

Ongoing management

The lead is secured to the skin, and a transparent dressing is applied. The patient is reevaluated. Daily care includes checking for infection, threshold testing, and evaluation of the paced surface ECG.

Complications

Sequelae of venous access

Depending on the site of venous access, a variety of adverse consequences may occur. Pneumothorax and hemothorax develop more frequently when subclavian access is performed.[8] Infection and thrombus formation most often occur after femoral vein access but may also develop when other access sites are used.

Thrombus formation at the venous access site is associated with embolic phenomena. As many as 60% of patients in whom thrombosis develops at the site of venous access exhibit evidence of pulmonary emboli on a ventilation-perfusion scan.[9] To prevent infection, femoral venous access should not be used for more than 24 hours. Significant bleeding after arterial puncture occurs more often when internal jugular access is used. Air embolism and nerve damage are the other potential complications.

Loss of capture and undersensing

The causes of loss of capture during transvenous pacing can be divided into the following two groups:

  • Causes related to the patient’s condition
  • Causes related to the lead position and the pacing unit

Hypoxia, acidosis, class I antiarrhythmic drugs, and electrolyte abnormalities are associated with an increased threshold and may result in loss of capture. In these cases, the main strategy should be treating the underlying cause while the output is temporarily increased to recapture the heart.

It is known that the site where the lead contacts the heart may exhibit some degree of inflammation and fibrosis. However, the output should be set to a value at least three times higher than the initial threshold to prevent loss of capture later. Inflammation and fibrosis still may be the cause of loss of capture.

Catheter dislodgment or fracture, poor endocardial contact, and perforation are other causes of loss of capture. The incidence of lead displacements is 1% in VVI pacemakers and 5.2% in DDD pacemakers (with 3.8% of the cases affecting atrial leads and 1.4% affecting ventricular leads).[10] Acceptable displacement rates should be less than 1% for ventricular leads and no more than 2-3% for atrial leads.[10]

To determine the cause of such displacements, chest radiography and ECG should be performed, and further evaluations should depend on the initial findings from these tests. Repositioning of the lead under fluoroscopic guidance may be necessary if any of the aforementioned problems is diagnosed. Occasionally, the generator may malfunction or battery depletion can occur, either of which can result in loss of capture. Similar problems can result in loss of sensing.

Oversensing

Oversensing may be due to sensing P waves, T waves, or myopotentials. The location of the lead should be checked because dislodgment and movement toward the tricuspid valve may result in P-wave sensing by the pacemaker. In addition, the sensitivity of the generator can be reduced by increasing the sensing threshold value to eliminate P-wave or T-wave oversensing. Myopotentials, which are another source of oversensing, can be diagnosed by checking the ECG when the patient moves.

The figure below provides an overview of appropriate ventricular and dual-chamber pacing and illustrates common related problems such as oversensing, undersensing, and loss of capture.

(A) Ventricular pacing during asystole. There is i (A) Ventricular pacing during asystole. There is increase in pacing voltage that eventually captures heart. (B) Atrioventricular (AV) sequential pacing. On fourth beat, atrium was paced, and because intrinsic ventricular activity happened before AV pacing interval, the pacemaker sensed it appropriately and did not fire. On fifth beat, intrinsic atrial activity is appropriately sensed by pacemaker, and pacemaker therefore did not pace atrium. This schematic tracing shows appropriate dual-chamber pacemaker function. (C) Ventricular pacing. Fourth pacing spike is not followed by any ventricular activity and does not capture (ie, loss of capture). (D) AV sequential pacing with fourth beat demonstrating undersensing dysfunction. On fourth beat, intrinsic QRS exists that was not sensed by pacemaker, and therefore pacemaker fired (pacemaker spike within intrinsic QRS can be seen); this could not capture heart because of being in refractory period of cardiomyocytes. (E) AV sequential pacing with oversensing problem on third beat. Pacemaker did not pace ventricle because of inappropriate sensing of intrinsic ventricular activity, which actually does not exist. Pacemaker picking up muscular potentials can be one reason for oversensing.

Ventricular arrhythmia

Insertion of the catheter into the RV is associated with ventricular arrhythmia. Nonsustained ventricular tachycardia (VT), a common finding during that procedure, is usually cured by withdrawing the catheter. Sustained VT or ventricular fibrillation (VF) is a more serious arrhythmic complication.

It must be remembered that patients who receive transvenous cardiac pacing often have an underlying disease (eg, myocardial ischemia, hypoxia, acidosis, or drug toxicity) that renders them more prone to the development of VT or VF. An external defibrillator should be available at the bedside during the insertion of the catheter. Manipulation of the RA can also produce a variety of supraventricular tachycardias.

Myocardial perforation

Nathan et al showed that myocardial perforation may occur in 2-20% of patients during endocardial pacing lead placement.[11] Depending on the location and size of the perforation, the clinical presentation may range from mild chest discomfort and shoulder pain to severe sharp chest pain, shortness of breath, and tamponade. Physical examination may reveal pericardial rub, distant heart sounds, pulsus paradoxus, skeletal muscle pacing, or failure to pace.

If ECG shows a change in the morphology of the paced QRS, then echocardiography should be performed. In such cases, the catheter should be withdrawn, and pericardiocentesis may become necessary.

 

Medication

Medication Summary

The first step in transvenous pacing is obtaining venous access. Before venous access is obtained, the subcutaneous tissue and area around the course of the needle should be anesthetized with lidocaine 1% or 2%, with or without epinephrine.

Topical Anesthetics

Class Summary

Topical anesthetic agents are indicated for pain relief.

Lidocaine (Anestafoam, Xylocaine, Lidoderm, Topicaine)

Lidocaine is an amide local anesthetic used in 1-2% concentration. The 1% preparation contains 10 mg of lidocaine for each 1 mL of solution; the 2% preparation contains 20 mg of lidocaine for each 1 mL of solution. Lidocaine inhibits depolarization of type C sensory neurons by blocking sodium channels.

To improve local anesthetic injection, cool the skin with ethyl chloride before injection. Use smaller-gauge needles (eg, 27 gauge or 30 gauge). Make sure the solution is at body temperature. Infiltrate very slowly to minimize the pain. The time from administration to onset of action is 2-5 minutes, and the effect lasts for 1.5-2 hours.