Transcutaneous Cardiac Pacing

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. Transcutaneous cardiac pacing allows fast, efficient, and noninvasive ventricular stimulation in conscious patients to treat symptomatic bradycardias, including atropine-resistant unstable bradycardia in the emergency department. ^[2]

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

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 ^[3] 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. ^{[4, 5]}

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 when it is temporarily used as a bridge to permanent pacing. 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). ^[6]

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. ^[7] 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. ^[8] In general, patients with out-of-hospital symptomatic bradycardia or bradyasystole have a high mortality. ^[9] Transcutaneous pacing usually carries a poorer prognosis in asystole than in bradycardia. ^[10]

Transcutaneous cardiac pacing is occasionally used to determine whether a patient requires permanent pacing (eg, if sinus bradycardia is found in a patient with hypotension). 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. ^[11]

Transcutaneous pacing also can be temporarily used in patients who received thrombolytic therapy for acute myocardial infarction ^[12] when the risk of bleeding from surgical incisions is high.

In general, transcutaneous pacing is a simple method of cadiac pacing that can be applied rapidly. It is, however, inconvenient to the patient and not very reliable. Therefore, it is used in emergency situations, during procedures when the patient is under anesthesia, or when the pacing indication is temporary and intermittently appears (eg intermittent episodes of heart block due to a reversible cause). For situations in which there is enough time to insert a transvenous wire and when pacing is required more often or for a longer time period, transvenous cardiac pacing is preferred.

Temporary pacing with ipsilateral transcutaneous lead implantation of an active-fixation right ventricular lead connected to an externalized pacemaker followed by antibiotic therapy may be an option for cardiac pacing for longer periods, such as in pacemaker-dependent patients with systemic cardiac implantation device (CIED) infection or for patients after transcatheter aortic valve implantation with transient heart block. ^{[13, 14]}

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).

Asymptomatic 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.

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).

This overshoot potential is followed by a prominent transient outward current of K⁺ (I_to) 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 (I_ks, I_kr, I_KUR) (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. ^[15] Other pharmacologic and metabolic factors may also affect the stimulation threshold.

Regardless of the presence of structural heart disease, transcutaneous cardiac pacing is associated with similar electrocardiographic (ECG) and hemodynamic responses to those of transvenous pacing. ^[16] Transcutaneous cardiac pacing also appears to produce greater lengthening of ventricular repolarization than conventional transvenous pacing, but there is less of an increase of ECG markers of ventricular dispersion of repolarization. ^[17]

 

Updated guidelines on cardiac pacing and cardiac resynchronization therapy (CRT) were published in August 2021 by the European Society of Cardiology (ESC) and European Heart Rhythm Association (EHRA) in Europace. ^{[18, 19]} Emphasis has been placed on patient-centered care, shared decision making, and appropriate workup/testing prior to pacemaker implantation.

New recommendations include those for pacing after syncope, pacing following transcatheter aortic valve implantation (TAVI), CRT for heart failure (HF) and for prevention of pacing-induced cardiomyopathy, and pacing in various infiltrative and inflammatory diseases of the heart, as well as in different cardiomyopathies. ^{[18, 19]} New sections include those on pacing the His bundle (HBP) and the left bundle branch (LBB), as well as on evaluation of suspected or documented bradycardia or conduction system disease.

Select Key Messages

Cardiac pacing

Cardiac pacing is indicated in patients with:

• Sinus node dysfunction (SND), including those with bradycardia–tachycardia type of SND, when symptoms are clearly attributed to bradyarrhythmia

• Sinus rhythm (SR) and permanent or paroxysmal third- or second-degree type 2 or high-degree atrioventricular block (AVB), irrespective of symptoms

Single-lead ventricular pacing is indicated in the setting of permanent atrial fibrillation (AF) and permanent or paroxysmal AVB.

In the setting of syncope and unexplained falls, determine the diagnosis using available diagnostic methods before considering pacemaker therapy.

Cardiac resynchronization therapy

CRT is recommended in patients with symptomatic HF and left ventricular (LV) ejection fraction (EF) ≤35% despite optimal medical therapy (OMT) who are in SR and have LBB block (LBBB) QRS morphology, when QRS duration is ≥150 ms. Consider CRT in these patients when QRS duration is 130–149 ms.

In the setting of non-LBBB QRS morphology, less convincing evidence exists for the benefit of CRT, especially with normal PR and QRS duration < 150 ms. CRT should not be used in patients with HF and QRS duration < 130 ms unless ventricular pacing is needed.

Consider CRT in those with permanent AF, symptomatic HF, LVEF ≤35%, and QRS ≥130 ms who remain in New York Heart Association (NYHA) class III or ambulatory IV despite OMT.

Consider AV junction (AVJ) ablation for those with AF and CRT when at least 90-95% effective biventricular pacing is not achievable.

For patients with high-degree AVB and an indication for cardiac pacing who have HF with reduced EF (HFrEF) (LVEF < 40%), the ESC/EHRA recommend CRT rather than right ventricular (RV) pacing.

His bundle pacing

HBP may:

• Result in normal or near-normal ventricular activation; it is an attractive alternative to RV pacing

• Be considered for select patients with AVB and LVEF >40%, who are anticipated to have >20% ventricular pacing

• Correct ventricular conduction in a subset of patients with LBBB; thus, it may be used in lieu of biventricular pacing for HBP-based CRT in select patients

In patients offered HBP, individual consideration should be given for implanting an RV lead used as “backup” for pacing. In patients treated with HBP, tailor the device programming to the specific requirements of HBP.

Consider implantation of a leadless pacemaker when no upper extremity venous access exists, when the risk of device pocket infection is particularly heightened, and in patients on hemodialysis.

TAVI, other surgeries, and perioperative considerations

Undergoing TAVI raises the risk of developing AVB. Base decisions regarding post-TAVI cardiac pacing on preexisting and new conduction disturbances. Consider ambulatory electrocardiographic (ECG) monitoring for 7-30 days or electrophysiologic studies (EPS) in post-TAVI patients who have new LBBB or progression of a preexisting conduction anomaly, but who do not yet have any indication for a pacemaker.

In patients undergoing surgery for endocarditis or tricuspid valve surgery who have or develop AVB under surgery, consider placing epicardial pacing leads during surgery.

To reduce the risk of complications:

• Administer preoperative antibiotics before cardiovascular implantable electronic device (CIED) procedures

• Chlorhexidine–alcohol should be preferred for skin antisepsis

• Attempt cephalic or axillary vein access as first choice

• Avoid heparin bridging in CIED procedures to minimize the risk of hematoma and pocket infection

• Consider use of an antibiotic-eluting envelope in CIED reintervention procedures to lower the infection risk

Radiation therapy can be offered to patients with a pacemaker or CRT—provided individualized treatment planning and risk stratification is done beforehand and the device is interrogated as recommended around the period of radiation therapy.

For more information, please go to Transvenous Cardiac Pacing and Cardiac Resynchronization Therapy.

Go to 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy: Developed by the Task Force on cardiac pacing and cardiac resynchronization therapy of the European Society of Cardiology (ESC) With the special contribution of the European Heart Rhythm Association (EHRA) for full details.