Transcutaneous Cardiac Pacing 

Updated: Dec 17, 2014
Author: Ali A Sovari, MD, FACP, FACC; Chief Editor: Richard A Lange, MD, MBA 



Temporary cardiac pacing can be implemented via the insertion or application of intracardiac, intraesophageal, or transcutaneous leads; this topic focuses on transcutaneous cardiac pacing. Newer techniques (eg, using transcutaneous ultrasound to stimulate the heart) are under investigation.[1] The goal in temporary cardiac pacing is to improve cardiac hemodynamics until the underlying problem resolves or a permanent pacing strategy is applied.

External defibrillators usually have a pacing capability, and, when an external pacemaker or a defibrillator is used, the pacing stimulus can be induced via 2 large transcutaneous patches; both patches may be applied to the chest, or 1 patch may be applied to the chest and the other to the back. The video below demonstrates transcutaneous cardiac pacing using a defibrillator.

Transcutaneous cardiac pacing in a patient with third-degree heart block. Video courtesy of Therese Canares, MD; Marleny Franco, MD; and Jonathan Valente, MD (Rhode Island Hospital, Brown University).

Although transcutaneous cardiac pacing can be quickly and safely performed by staff members who do not have extensive training, many patients tolerate the pacing poorly, and the incidence of cardiac capture varies.

When compared with sinus rhythm or atrioventricular (AV) sequential pacing, transcutaneous cardiac pacing is associated with reduced left ventricular systolic pressure and a lower stroke index[2] because of AV dyssynchrony. However, perhaps because of associated diaphragmatic and skeletal muscle contractions, transcutaneous pacing can provide greater cardiac output than endocardial ventricular pacing does.[3, 4]


Transcutaneous cardiac pacing (the fastest method of cardiac pacing) can be used until permanent pacing becomes available. Therefore, all indications for permanent cardiac pacing are considered indications for transcutaneous pacing as well. Indications for permanent cardiac pacing, along with the corresponding levels of supporting evidence, are well summarized by the American College of Cardiology (ACC) and the American Heart Association (AHA).[5]

Temporary pacing is appropriate when a permanent pacing device must be replaced, repaired, or changed, and when permanent pacing fails. However, in some of those situations, other methods of temporary pacing (eg, transvenous pacing) may be more appropriate.

Because transcutaneous pacing is a temporary method of cardiac pacing, it may be indicated for the treatment of a reversible condition for which permanent pacing is contraindicated. For instance, Ho et al have reported using transcutaneous pacing in patients with bradycardia due to hypothermia.[6] Other examples of reversible conditions that may require temporary cardiac pacing include the following:

  • Injury to the sinus node or other parts of the conduction system after cardiac surgery - Injuries after coronary bypass surgery tend to be temporary, whereas injuries after valve surgery or cardiac transplantation may not be reversible

  • Chest and cardiac trauma associated with temporary sinus node or AV node dysfunction

  • Metabolic and electrolyte derangements (eg, hyperkalemia)

  • Right-heart catheterization in a patient with a left bundle-branch block or intraventricular conduction delay - This may be associated with temporary complete heart block, in which case transcutaneous cardiac pacing is indicated

  • Drug-induced bradyarrhythmia (eg, digitalis toxicity) - If the drug should be continued and there is no alternative, consider permanent pacing

  • Other diseases that may be associated with temporary damage to the sinus or AV node (eg, Lyme disease or bacterial endocarditis)

Transcutaneous pacing is also part of advanced cardiac life support measures used in patients whose recorded cardiac rhythm reflects bradycardia or asystole. However, the available evidence is insufficient to prove the efficacy of prehospital transcutaneous pacing in cases of symptomatic bradycardia and bradyasystolic arrest.[7] In general, patients with out-of-hospital symptomatic bradycardia or bradyasystole have a high mortality.[8] Transcutaneous pacing usually carries a poorer prognosis in asystole than in bradycardia.[9]

Transcutaneous cardiac pacing is occasionally used to determine whether a patient requires permanent pacing (eg, if marked sinus bradycardia or a severe first-degree AV block are found in a patient with a history of frequent syncope). However, such patients who undergo cardiac pacing may become pacemaker-dependent and exhibit asystole when the pacing is terminated, even though they may not have experienced asystole in the absence of pacing.

Although transcutaneous 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 various atrial and ventricular tachycardias (eg, postoperative atrial flutter and monomorphic ventricular tachycardia). Pacing also may be used to prevent bradycardia-dependent tachycardias (eg, torsades de pointes).

In one study, Im et al prophylactically used transcutaneous pacing for expected bradycardia during carotid stenting; this appeared to be safe and effective in preventing intraprocedural bradycardia and hypotension, with a decrease in additional pharmacologic support during the procedures.[10]

Transcutaneous pacing also becomes the pacing method of choice in patients who received thrombolytic therapy for acute myocardial infarction[11] when the risk of bleeding from surgical incisions is high.

Temporary pacing with ipsilateral transcutaneous lead implantation of an active-fixation right ventricular lead connected to externalized pacemaker followed by antibiotic therapy may be an option for pacemaker-dependent patients with systemic cardiac implantation device (CIED) infection.[20]


In general, temporary transcutaneous cardiac pacing should not be considered for asymptomatic patients with a fairly stable rhythm (eg, first-degree AV block, Mobitz I, or a stable escape rhythm). For example, pacing an asymptomatic patient with a stable escape rhythm may render him or her pacing-dependent, and withholding pacing can then cause asystole. Although these rhythms are generally stable, there are exceptions (eg, Mobitz I with a wide QRS may indicate infra–AV nodal delay and thus may progress to complete heart block).

Bradyarrhythmias secondary to profound hypothermia typically do not warrant pacing, and the electrical stimulation of pacing may cause them to degenerate into more life-threatening arrhythmias.

Technical Considerations

The sinoatrial (SA) node, located in the high right atrium close to the entrance of the superior vena cava, is the natural pacemaker of the heart and initiates the impulse in normal sinus rhythm. The impulse propagates from the right atrium to the left atrium and then to the AV node. The AV node, which is the only electrical connection between the atria and the ventricles in a normal heart, conveys the impulse with a delay to the His bundle.

From the His bundle, the impulse propagates to the right bundle branch and the left bundle branch; the latter, in turn, divides into the left anterior and posterior fascicles. The Purkinje fibers, which are smaller branches of the conduction system, convey electrical activity to the myocardium. Very rapid impulse propagation in the conduction system facilitates the simultaneous depolarization (and therefore the simultaneous contraction) of the ventricles.

A myocyte has a lipid bilayer membrane. At rest, the inside of a myocyte membrane has a more negative charge (about –90 mV, the so-called resting membrane potential) than the outside of the membrane. The lipid bilayer membrane is impermeable to most ions. Sodium-potassium adenosine triphosphatase (Na+/K+ -ATPase) in the membrane exports 3 Na+ from the cell and imports 2 K+ into the cell; this results in a negative charge inside the membrane.

When the myocyte membrane is at rest (ie, when the cytosolic Ca2+ concentration is low), the Na+/Ca2+ pump contributes to the negative charge inside the membrane by exporting 3 Na+ and importing 1 Ca2+. The net result is a higher concentration of Na+ outside the cell, a higher concentration of K+ inside the cell, and a negative resting membrane potential.

Other ion channels in the membrane are inactive at –90 mV; however, they are activated at a relatively higher membrane voltage. For example, if a stimulus depolarizes the membrane to the threshold potential, which is usually about –70 mV, then rapid opening of the Na+ channels enables the free movement of a large number of Na+ ions that quickly depolarize the cell membrane to approximately +20 mV and initiate an action potential (phase 0) (see the image below).

Normal action potential of myocyte and main ion ch Normal action potential of myocyte and main ion channels that play major roles in different phases of action potential.

This overshoot potential is followed by a prominent transient outward current of K+ (Ito) that reduces the membrane potential and creates a notch on the action potential (phase 1). The myocyte then enters the plateau phase, in which the inward Ca2+ current is almost equal to all outward K+ currents (Iks, Ikr, IKUR) (phase 2).

In the next phase of action potential, during which all inward currents stop, the outward K+ currents continue to repolarize the cell membrane (phase 3). In that phase of action potential (the relative refractory period), the cell may depolarize again if a strong enough stimulus occurs. Finally, the myocyte enters the resting phase (phase 4), during which it can be fully excited again.

In the pacemaker cells of the heart, the membrane potential at rest gradually increases until it reaches the threshold potential and causes automatic depolarization (automaticity). The propagation of an impulse from myocyte to myocyte is both a passive and an active process. Gap junctions between myocytes have an important role in transmitting action potentials.

An artificial electrical pacing stimulus in the heart induces a propagating wave of cardiac action potentials. For a pacing stimulus to create a self-regenerating wave of action potentials, it must be applied with adequate intensity for a sufficient period of time. The duration and intensity of the pacing impulse are important factors in the capture of the pacing stimulus.

In addition, very rapid pacing with a short interval can increase the pacing threshold by delivering the pacing stimulus during the relative refractory period of myocytes.[12] Other pharmacologic and metabolic factors may also affect the stimulation threshold.


Periprocedural Care

Patient Education and Consent

Appropriately used, external cardiac pacing is associated with few complications. Skin burns, pain, discomfort, and failure to capture are the main limitations of this method. It is important to educate the patient about the procedure and especially about potential discomfort related to skin tingling and burning and associated skeletal muscle contractions. If time allows, obtain informed consent.


Equipment used in transcutaneous cardiac pacing includes the following:

  • Pacing unit

  • Cardiac monitor

  • Defibrillator (see the image below)

  • Pacing electrodes (pads)

    Defibrillator with pacing capability. Defibrillator with pacing capability.

Although some pacing units provide only pacing, most defibrillators provide both cardiac pacing and rhythm monitoring. Those units can usually deliver a current as high as 200 mA for as long as 40 ms. The stimulus current is usually delivered in a rectangular waveform, which has been shown to be associated with lower excitation thresholds than other impulse shapes.[13]

The size of the electrode pads usually ranges from 8-15 cm, and the pacing electrodes can be applied by medical personnel. Chest pressure can be applied and cardiopulmonary resuscitation performed by pressing on the pads. To record a clear electrocardiographic rhythm, the recording electrode should be placed as far as possible from the pacing pads (see Positioning).

External pacemakers

Transcutaneous pacing with external pacemakers is indicated as a temporizing measure for treatment of symptomatic bradycardias, including sinus bradycardias and atrioventricular (AV) nodal blocks; it may also be used prophylactically in patients with these rhythms who are maintaining a stable blood pressure. External transcutaneous pacing has been used successfully for overdrive pacing of tachyarrhythmias; however, it is not considered beneficial in the treatment of asystole.

Modern external pacemakers use longer pulse durations and larger electrodes than the early models did. These modifications allow administration of higher currents with less patient discomfort. Studies have demonstrated that more than 90% of patients tolerate pacing for 15 or more minutes. Modern devices are capable of delivering up to 140-200 mA tolerably.

Patient Preparation


Transcutaneous cardiac pacing may be associated with discomfort such as a burning sensation of the skin, skeletal muscle contractions, or both. Because of this, patients who are conscious and hemodynamically stable should be sedated with a drug, such as midazolam, before initiation of pacing (see Procedural Sedation).

The literature reports a wide range of sedation techniques and sedative agents. Combination sedation with benzodiazepines and narcotics appear to be in relatively broad use.[19]


Before applying the pacing electrodes, wipe the patient’s skin with alcohol, and allow the area to dry. Without abrading the skin, carefully shave excessive body hair, which can elevate the pacing threshold and increase burning and discomfort.

Skin abrasions, the presence of a foreign body beneath the electrodes, sweating, and a high pacing threshold increase the patient’s pain and discomfort. Try to avoid abrading the skin when shaving excess hair, to remove a foreign body, to clean the skin, and to review and address the above-mentioned factors that may increase the pacing threshold.

The anterior electrode should have negative polarity and should be placed either over the cardiac apex or at the position of lead V3. If the positive electrode is placed anteriorly, the pacing threshold may increase significantly; this, in turn, increases the patient’s discomfort and may result in failure to capture.

The posterior electrode, which should be of positive polarity, should be placed inferior to the scapula or between the right or left scapula and the spine; it should not be placed over the scapula or the spine. Alternatively, the positive electrode can be placed anteriorly on the right upper part of the chest (see the image below). The latter configuration does not affect the pacing threshold.[12]

Pacing electrode pads of external pacing unit and Pacing electrode pads of external pacing unit and locations in which each pad should be placed.


Transcutaneous Pacing

The video below demonstrates transcutaneous cardiac pacing using a defibrillator.

Transcutaneous cardiac pacing in a patient with third-degree heart block. Video courtesy of Therese Canares, MD; Marleny Franco, MD; and Jonathan Valente, MD (Rhode Island Hospital, Brown University).

In nonemergent situations, sedate the patient. Record the baseline rhythm and vital signs, if this has not already been done.

Prepare and apply the pads as described earlier (see Positioning). Although transcutaneous pacing has been used continuously for as long as 4-5 days,[14, 15] the sites at which the pads are applied should be changed every 4-5 hours to reduce skin burn and discomfort. For patients who require longer-term pacing, a more appropriate mode of pacing should be considered.

Turn the pacemaker on, and choose the pacing mode. Most pacing units are capable of pacing on either a demand mode or a fixed mode. The demand mode is usually preferable and should be used initially. If capture cannot be obtained on that mode, then the fixed mode should be tried. In the demand mode, the pacemaker senses the intrinsic impulses and delivers current only if necessary.

Capture the heart rate. If the patient is in cardiac arrest with bradycardia or an asystolic rhythm, the pacing should be initiated at the maximum current output to ensure that capture is achieved as soon as possible, after which time the current can be gradually reduced to 5-10 mA above the threshold.

The presence of 1 QRS complex after each pacing stimulus suggests but does not confirm the capture. Cardiac capture should be confirmed by detecting the pulse (see the image below). However, pulse detection can be difficult, particularly in bradyasystolic arrest; in these cases, detecting ventricular capture by means of 2-dimensional echocardiography is a good alternative if the echocardiography system is available.[16, 17]

Rhythm strip showing failure to capture in first 4 Rhythm strip showing failure to capture in first 4 pacing stimuli that did not produce any pulse. When capture occurred, each pacing artifact is followed by QRS complex (albeit bizarrely shaped) and pulse.

A small polarization artifact that is usually noted after each pacing artifact should not be confused with a QRS complex. In a healthy individual, the pacing threshold is usually less than 80 mA.

Many factors (eg, obesity, myocardial ischemia, metabolic derangement, pneumothorax, poor skin-to-electrode contact) can increase the pacing threshold, and some of those conditions are correctable. Reevaluate the patient.

It has been shown that walkie-talkies and cellular digital phones can cause various disturbances in the function of external pacing units, including pacing inhibition and asynchronous pacing,[18] even when these devices are as far as 200 cm from the pacing units. Therefore, an appropriate warning against using such communication equipment near patients undergoing transcutaneous cardiac pacing should be issued.



Medication Summary

The goal of pharmacotherapy is to provide sedation to relieve the discomfort, such as burning sensation of the skin and/or skeletal muscle contractions that are associated with transcutaneous cardiac pacing.

Anxiolytics, Benzodiazepines

Class Summary

Anxiolyticsare used to sedate patients who are conscious and hemodynamically stable, before initiation of pacing.


Midazolam is a shorter-acting benzodiazepine sedative-hypnotic useful in patients requiring acute and/or short-term sedation. Midazolam is also useful for its amnestic effects.