Transvenous Cardiac Pacing Technique

Updated: Feb 19, 2016
  • Author: Ali A Sovari, MD, FACP, FACC; Chief Editor: Vincent Lopez Rowe, MD  more...
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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.

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 It is then withdrawn to the superior vena cava (SVC) while being rotated anteriorly to permit advancement into the right atrial appendage.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, [5] 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 msec, 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 right ventricle.

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 right ventricular 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 right ventricular 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.



Transvenous cardiac pacing may be associated with a number of different complications, as follows.

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. [6] 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. [7] 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 two groups: those related to the patient’s condition and those 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% ventricular leads). [8] Acceptable displacement rates should be less than 1% for ventricular leads and no more than 2-3% for atrial leads. [8]

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 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. [9] 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.