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.  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.
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  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). 
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.  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
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.  In general, patients with out-of-hospital symptomatic bradycardia or bradyasystole have a high mortality.  Transcutaneous pacing usually carries a poorer prognosis in asystole than in bradycardia. 
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. 
Transcutaneous pacing also becomes the pacing method of choice in patients who received thrombolytic therapy for acute myocardial infarction  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. 
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.
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+ (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.  Other pharmacologic and metabolic factors may also affect the stimulation threshold.