The most common indication for temporary pacing in the ICU setting is a hemodynamically significant or symptomatic bradyarrhythmia such as sinus bradycardia or high-grade atrioventricular (AV) block.

Sinus bradycardia and AV block are commonly seen in patients with acute coronary syndromes, hyperkalemia, myxedema, or increased intracranial pressure. Infectious processes such as endocarditis or Lyme disease [6] may impair AV conduction. Bradyarrhythmias also result from treatment or intoxication with digitalis, antiarrhythmic, beta-blocker, or calcium channel blocker medications and may also result from exaggerated vasovagal reactions to ICU procedures such as suctioning of the tracheobronchial tree in the intubated patient. Bradycardia-dependent ventricular tachycardia may occur in association with ischemic heart disease.

Temporary cardiac pacing is used less often for the prevention and termination of supraventricular and ventricular tachyarrhythmias.

Atrial pacing may be effective in terminating atrial flutter and paroxysmal nodal supraventricular tachycardia [7,8]. Atrial pacing in the ICU setting is most frequently performed when temporary epicardial electrodes have been placed during cardiac surgery. A critical pacing rate (usually 125% to 135% of the flutter rate) and pacing duration (usually about 10 seconds) are important in the successful conversion of atrial flutter to sinus rhythm.

In some clinical situations, pacing termination of atrial flutter may be preferable to synchronized cardioversion, which requires sedation with its attendant risks. Pacing termination is the treatment of choice for atrial flutter in patients with epicardial atrial wires in place after cardiac surgery. It may be preferred as the means to convert atrial flutter in patients on digoxin and those with sick sinus syndrome, as these groups often demonstrate prolonged sinus pauses after DC cardioversion.

Temporary pacing may be required for the prevention of paroxysmal polymorphic ventricular tachycardia in patients with prolonged QT intervals (torsades de pointes), particularly when secondary to drugs [9,10]. Temporary cardiac pacing is the treatment of choice to stabilize the patient while a type I antiarrhythmic agent exacerbating ventricular irritability is metabolized. In this situation, the pacing rate is set to provide a mild tachycardia. The effectiveness of cardiac pacing probably relates to decreasing the dispersion of refractoriness of the ventricular myocardium (shortening the QT interval).

Temporary ventricular pacing may be successful in terminating ventricular tachycardia. If ventricular tachycardia must be terminated urgently, cardioversion is mandated (Chapter 6). However, in less urgent situations, conversion of ventricular tachycardia via rapid ventricular pacing may be useful. The success of this technique depends on the setting in which ventricular tachycardia occurs. “Overdrive” ventricular pacing is often effective in terminating monomorphic ventricular tachycardia in a patient with remote myocardial infarction or in the absence of heart disease. This technique is less effective when ventricular tachycardia complicates acute myocardial infarction or cardiomyopathy. Rapid ventricular pacing is most successful in terminating ventricular tachycardia when the ventricle can be “captured” (asynchronous pacing for 5 to 10 beats at a rate of 50 beats per minute greater than that of the underlying tachycardia). Extreme caution is advised, as pacing may result in acceleration of ventricular tachycardia or degeneration to ventricular fibrillation; a cardiac defibrillator should be immediately available at the bedside.

Some of the many transvenous pacing catheters available for use in the critical care setting are illustrated in Figure 5.1. Pacing catheters range in size from 4 Fr (1.2 mm) to 7 Fr (2.1 mm). In urgent situations, or where fluoroscopy is unavailable, a flow-directed flexible balloon-tipped catheter (Fig. 5.1, top) may be placed in the right ventricle using ECG guidance. After gaining access to the central venous circulation, the catheter is passed into the vein and the balloon inflated. After advancing the catheter into the right ventricle, the balloon can be deflated and the catheter tip advanced to the right ventricular apex. Although the balloon-tipped catheter may avoid the need for fluoroscopy, placement may be ineffective in the setting of low blood flow during cardiac arrest or in the presence of severe tricuspid regurgitation. Stiff catheters (Fig. 5.1, middle) are easier to manipulate but require insertion under fluoroscopic guidance.

A flexible J-shaped catheter (Fig. 5.1, bottom), designed for temporary atrial pacing, is also available [23]. This lead is positioned by “hooking” it in the right atrial appendage under fluoroscopic guidance, providing stable contact with the atrial endocardium. Either the subclavian or internal jugular venous approach may be used.

A multilumen pulmonary artery catheter is available with a right ventricular lumen. Placement of a small (2.4 Fr) bipolar pacing lead through the right ventricular lumen allows intracardiac pressure monitoring and pacing through a single catheter [24]. Details on its use and insertion are described in Chapter 4.

An esophageal “pill” electrode allows atrial pacing and recording of atrial depolarizations without requiring central venous


cannulation. As mentioned earlier, detecting atrial depolarization aids in the diagnosis of tachyarrhythmias. Esophageal pacing has also been used to terminate supraventricular tachycardia and atrial flutter [25]. Because the electrode can be uncomfortable and may not give consistent, stable capture, the esophageal electrode is typically limited to short-term use for diagnosis of arrhythmias in pediatric patients.