Emergency Cardiac Pacing

The purpose of cardiac pacing is to restore or ensure effective cardiac depolarization. Emergency cardiac pacing may be instituted either prophylactically or therapeutically. Prophylactic indications include patients with a high risk for atrioventricular (AV) block. Therapeutic indications include symptomatic bradyarrhythmias and overdrive pacing. Pacing for asystole has very minimal success but it has been used for this condition. Several approaches to pacing can be taken, including transcutaneous, transvenous, transthoracic, epicardial, endocardial, and esophageal. Transcutaneous and transvenous pacemakers are the two techniques most commonly used in the emergency department (ED). Because it can be instituted quickly and noninvasively, transcutaneous pacing is the technique of choice in the ED when time is of the essence. Transvenous pacing should be reserved for patients who require prolonged pacing or have a very high (>30%) risk for heart block. Transcutaneous pacing is generally a temporizing measure that may precede transvenous cardiac pacing. Although it is not an expectation that all emergency clinicians will be adept at placing temporary transvenous cardiac pacemakers, many have mastered the techniques and are often the only clinicians available to perform this lifesaving procedure.

Emergency Transvenous Cardiac Pacing

The transvenous method of endocardial pacing is commonly used and is both safe and effective. In skilled hands, the semifloating transvenous catheter is successfully placed under electrocardiographic (ECG) guidance in 80% of patients. The technique can be performed in less than 20 minutes in 72% of patients and in less than 5 minutes in 30% ( – ). However, in some instances, anatomic, logistic, and hemodynamic impediments can prohibit successful pacing by even the most skilled clinician. As with other medical procedures, it should not be performed without a thorough understanding of its indications, contraindications, and complications.

Because this procedure is essentially performed in a blind manner, sometimes it will not be successful. This may be because the condition is not amenable to pacing (e.g., asystole, drug overdose) or because of technical difficulties inherent with the procedure.

Review Box15.1, Transvenous cardiac pacing: indications, contraindications, complications, and equipment.

Background

The ability of muscle to be artificially depolarized was recognized as early as the 18th century. Initial efforts focused on the transcutaneous approach (see later in this section). Over the succeeding years several scattered experiments were reported, and in 1951 Callaghan and Bigelow first used the transvenous approach to stimulate asystolic hearts in hypothermic dogs.

Furman and Robinson demonstrated the transvenous endocardial approach in humans in 1958. They treated two patients with complete heart block and Stokes-Adams seizures, thus reconfirming that low-voltage pacing could completely control myocardial depolarization. The catheter remained in the second patient for 96 days without complication. Other early clinical studies also demonstrated the utility of transvenous pacing. Fluoroscopic guidance was used for placement of the pacing catheter in all these studies.

In 1964 Vogel and coworkers demonstrated the use of a flexible catheter passed without fluoroscopic guidance for intracardiac electrocardiography. One year later, Kimball and Killip used this technique to insert endocardial pacemakers at the bedside. They noted technical problems in 20% of their patients, including intermittent capture, difficulty passing the catheter, and catheter knotting. During the same year, Harris and colleagues confirmed the ease and speed with which this procedure could be accomplished.

Before 1965 all intracardiac pacing was done asynchronously, which meant that the pacing catheter could cause electrical stimulation during any phase of the cardiac cycle. Asynchronous pacing frequently resulted in the pacemaker firing during the vulnerable period of an intrinsic depolarization; this occasionally caused ventricular tachycardia or fibrillation. In 1967 a demand pacemaker generator that sensed intrinsic depolarizations and inhibited the pacemaker for a predetermined period was used successfully by Zuckerman and associates in six patients. Since then there has been steady progress in the design and functionality of pacemakers. Table 15.1 summarizes the four-letter code that is used to describe modern pacemakers (there is a fifth letter for combined pacemaker-cardioverter/defibrillators). The most commonly used emergency transvenous pacemaker is represented by the code VVI: the ventricle is paced, the ventricle is sensed, and when a native impulse is sensed, the pacemaker is inhibited. Dual-chamber pacing (DDD or DDDR) is the preferred methodology for permanent pacing but is rarely used on an emergency basis because of the increased complexity of the procedure.

TABLE 15.1

Four-Letter Pacemaker Code

FIRST LETTER	SECOND LETTER	THIRD LETTER	FOURTH LETTER
Chamber Paced	Chamber Sensed	Sensing Response	Programmability
A = Atrium	A = Atrium	T = Triggered	P = Simple
V = Ventricle	V = Ventricle	I = Inhibited	M = Multiprogrammable
D = Dual	D = Dual	D = Dual (A triggered and V inhibited)	R = Rate adaptive
O = None	O = None	O = None	C = Communicating
			O = None

Rosenberg and coworkers introduced an improved pacing catheter known as the Elecath semifloating pacing wire. The Elecath was stiffer than the Flexon steel wire electrode that was in prevailing use. Rosenberg and coworkers achieved pacing in 72% of their patients with an average procedure time of 18 minutes. They also noted that 30% of their patients were paced in 5 minutes or less. In 1970, Swan and Ganz introduced the technique of heart catheterization with a flow-directed balloon-tipped catheter. Schnitzler and colleagues successfully used this method for placement of a right ventricular pacemaker in 15 of 17 patients.

In 1981 Lang and associates compared bedside use of the flow-directed balloon-tipped catheter with insertion of a semirigid electrode catheter in 111 perfusing patients. These researchers found a significantly shorter insertion time (6 minutes 45 seconds versus 13 minutes 30 seconds), a lower incidence of serious arrhythmias (1.5% versus 20.4%), and a lower incidence of catheter displacement (13.4% versus 32%) with the balloon-tipped catheter. They concluded that the balloon-tipped catheter was the method of choice for temporary transvenous pacing.

Although placing temporary transvenous pacemakers has long been considered a core skill in the ED, it has not been well studied. Birkhahn and coworkers retrospectively compared the experience of emergency physicians with that of cardiologists in placing transvenous pacemakers under ECG guidance. They reported a 13% risk for major complications in both groups of specialists. They concluded that pacemaker placement by emergency physicians under ECG guidance without fluoroscopy had success and complication rates that were comparable to those of their cardiology colleagues. In a retrospective review of 43 ED patients in whom emergency transvenous pacemaker placement was attempted, there was a 95% success rate and no immediate or delayed complications.

Indications

The purpose of cardiac pacing is to stimulate effective cardiac depolarization. In most cases the specific indications for cardiac pacing are clear; however, some areas are still controversial. The decision to pace on an emergency basis requires knowledge of the presence or absence of hemodynamic compromise, the cause of the rhythm disturbance, the status of the AV conduction system, and the type of dysrhythmia. The clinician caring for the patient is in the best position to decide on the value or nonvalue of pacing, based on nuances of the clinical scenario that are not possible to unravel by any theoretical discussion. Controversy exists throughout the literature, and this discussion is not meant to set a standard of care for individual circumstances.

In general, the indications can be grouped into those that cause either tachycardias or bradycardias (see Review Box 15.1 ). Transcutaneous cardiac pacing (TCP) has become the mainstay of emergency cardiac pacing and is often used pending placement of a transvenous catheter or to determine whether potentially terminal bradyasystolic rhythms will respond to pacing.

Bradycardias

Sinus Node Dysfunction

Sinus node dysfunction may be manifested as sinus arrest, tachybrady (sick sinus) syndrome, or sinus bradycardia. Although symptomatic sinus node dysfunction is a common indication for elective permanent pacing, it is seldom cause for emergency pacemaker insertion.

Seventeen percent of patients with acute myocardial infarction (AMI) will experience sinus bradycardia. It occurs more frequently with inferior than with anterior infarction and has a relatively good prognosis when accompanied by a hemodynamically tolerable escape rhythm. However, sinus bradycardia is not a benign rhythm in this situation; it has a mortality rate of 2% with inferior infarction and 9% with anterior infarction. Sinus node dysfunction frequently responds to medical therapy but requires prompt pacing if such therapy fails.

Asystolic Arrest

Transvenous pacing in an asystolic or bradyasystolic patient has little value and is not recommended. In a study of 13 patients who had suffered cardiac arrest, capture of the myocardium was noted in 4 patients, but there were no survivors. Transvenous pacing alone may also not be effective for post-countershock pulseless bradyarrhythmias. This failure of pacing has likewise been demonstrated with transcutaneous pacemakers, thus suggesting that failure of effective pacing is primarily related to the state of the myocardial tissue. Cardiac pacing may be used as a “last-ditch” effort in bradyasystolic patients but is rarely successful and is not considered standard practice. Early pacing is essential when done for this purpose if success is to be achieved (see later in this section). Most importantly, given the continued emphasis on the importance of maximizing chest compressions during cardiopulmonary resuscitation (CPR), interrupting CPR to institute emergency pacing is not recommended.

AV Block

AV block is the classic indication for pacemaker therapy. In symptomatic patients without myocardial infarction (MI) and in asymptomatic patients with a ventricular rate lower than 40 beats/min, pacemaker therapy is indicated.

In patients with AMI, 15% to 19% progress to heart block: first-degree block develops in approximately 8%, second-degree block in 5%, and third-degree block in 6%. First-degree block progresses to second- or third-degree block 33% of the time, and second-degree block progresses to third-degree block approximately one-third of the time.

AV block occurring during anterior infarction is believed to result from diffuse ischemia in the septum and infranodal conduction tissue. Because these patients tend to progress to high-degree block without warning, a pacemaker is often placed prophylactically. Some patients are prophylactically paced on a temporary basis, even in the absence of hemodynamic compromise.

During inferior infarction, early septal ischemia is the exception and typically block develops sequentially from first-degree to Mobitz type I second-degree and then to third-degree AV block. These conduction abnormalities frequently result in hemodynamically tolerable escape rhythms because of sparing of the bundle branches. A hemodynamically unstable patient who is unresponsive to medical therapy should be paced promptly. Whether and when stable patients should be paced is unclear, but placing a transcutaneous pacer is one option that can be attempted before placing a transvenous pacing catheter.

Trauma

Pacing is not a standard intervention in traumatic cardiac arrest, but in selected cases it may be considered. Several rhythm and conduction disturbances have been documented in patients with nonpenetrating chest trauma. In these patients, traumatic injury to the specialized conduction system may predispose to life-threatening dysrhythmias and blocks that can be treated by cardiac pacing.

Hypovolemia and hypotension can cause ischemia of conduction tissue and cardiac dysfunction. Marked bradyarrhythmias that persist even after vigorous volume replacement may rarely respond to cardiac pacing in patients with such trauma.

Bundle Branch Block and Ischemia

Bundle branch block occurring in AMI is associated with a higher mortality rate and a greater incidence of third-degree heart block than is an uncomplicated infarction. Atkins and colleagues noted that 18% of patients with MI had a bundle branch block. Of these patients, complete heart block developed in 43% who had right bundle branch block (RBBB) and left axis deviation, in 17% who had left bundle branch block (LBBB), in 19% who had left anterior hemiblock, and in 6% who had no conduction block. The investigators concluded that RBBB with left axis deviation should be paced prophylactically.

A study by Hindman and associates confirmed the natural history of bundle branch block during MI. In their study, the presence or absence of first-degree AV block, the type of bundle branch block, and the age of the block (new versus old) were used to determine the relative risk for progression to type II second-degree or third-degree block ( Table 15.2 ).

TABLE 15.2

Influence of Different Variables on the Risk for High-Degree Atrioventricular Block in Patients With Bundle Branch Block During Myocardial Infarction

From Hindman MC, Wagner GS, JaRo M, et al: The clinical significance of bundle branch block complicating acute myocardial infarction. 2. Indications of temporary and permanent pacemaker insertion, Circulation 58:690, 1978.

PATIENTS	PROGRESSING TO HIGH-DEGREE AVB (%)
Infarct location
Anterior	25
Indeterminate	12
Inferior or posterior	20
PR interval
>0.20 sec	25
≤0.20 sec	19
Type of BBB
LBBB	13
RBBB	14
RBBB + LAFB	27
RBBB + LPFB	29
ABBB	44
Onset of BBB
Definitely old	13
Possibly new	25
Probably new	26
Definitely new	23

ABBB, Alternating bundle branch block; AVB, atrioventricular block; BBB, bundle branch block; LAFB, left anterior fascicular hemiblock; LBBB, left bundle branch block; LPFB, left posterior fascicular hemiblock; RBBB, right bundle branch block.

Because of the increased risk, consider pacing for the following conduction blocks: new-onset LBBB, RBBB with left axis deviation or other bifascicular block, and alternating bundle branch block. Though controversial, one authority recommends prophylactic pacing for all new bundle branch blocks when MI is evident.

Whether to place a transvenous pacemaker prophylactically in patients with LBBB before insertion of a flow-directed pulmonary artery catheter (PAC) remains controversial. Some researchers strongly advocate this procedure because of the risk for transient RBBB and life-threatening complete heart block associated with PAC placement. One study noted that this risk is low in patients with previous LBBB but continued to recommend temporary catheter placement for all cases of new LBBB. One solution to this problem is to place a transcutaneous pacemaker before catheterization as an emergency measure should heart block develop. In these cases a temporary transvenous pacemaker can be placed in a semi-elective manner when needed. In any event, the trend toward decreased PAC use, particularly outside the critical care setting, makes it unlikely that this will be an issue in the ED.

Most of the studies investigating temporary pacing in the setting of AMI were done in the era before the use of thrombolytic agents or percutaneous coronary intervention. Nonetheless, whereas modern treatment of AMI has reduced the frequency of emergency transvenous pacemaker insertion, the indications are essentially unchanged and it remains a potentially life-saving intervention.

Tachycardias

Hemodynamically compromising tachycardias are usually treated with medications or electrical cardioversion. Since 1980 there has been increasing interest in pacing therapy for symptomatic tachycardias. Supraventricular dysrhythmias, with the exception of atrial fibrillation, respond well to atrial pacing. By “overdrive” pacing the atria at rates 10 to 20 beats/min faster than the underlying rhythm, the atria become entrained, and when the rate is slowed the rhythm frequently returns to normal sinus. A similar procedure is done for ventricular dysrhythmias. Overdrive pacing is especially useful for arrhythmias with recurrent prolonged QT intervals, such as those seen with quinidine toxicity or torsades de pointes. Though an attractive thought, there is no reported experience with these techniques in the ED. Transvenous pacing is also useful in patients with digitalis-induced dysrhythmias, in whom direct current cardioversion may be dangerous, or in patients in whom there is further concern about myocardial depression with drugs.

Cardiac Pacing for Drug-Induced Dysrhythmias

Significant dysrhythmias can be caused by excessive therapeutic medication (often in combination therapy) and overdose of cardioactive medications. Because these drugs have direct effects on cells of the myocardial pacemaker and conduction system, cardiac pacing is usually of little therapeutic value. Both bradycardias and tachycardias may result. Tachycardic rhythms from amphetamines, cocaine, anticholinergics, cyclic antidepressants, theophylline, and other drugs do not benefit from cardiac pacing. Drug-induced torsades de pointes may theoretically be overdriven by pacing, but data on this technique are lacking. Any drug that affects the central nervous system (e.g., opiates, sedative-hypnotics, clonidine) may produce bradycardia. Uncommon causes of toxin-induced bradycardia include organophosphate poisoning, various cholinergic drugs, ciguatera poisoning, and rarely, plant toxins. Cardiac pacing is not used for bradycardias from these sources; rather, the underlying central nervous system depression is addressed.

Severe bradycardia and heart block often accompany overdose of digitalis preparations, β-adrenergic blockers, and calcium channel blockers. Although intuitively attractive, cardiac pacing is not generally effective for serious toxin-induced bradycardias, even though there have been rare case reports of success. In β-blocker overdose, pacing may increase the heart rate but rarely benefits blood pressure or cardiac output. Worsening of blood pressure may occur as a result of loss of atrial contractions with ventricular pacing. Likewise, calcium channel blocker overdose and digitalis-induced bradycardia and heart block rarely benefit from cardiac pacing. Pharmacologic interventions, such as digoxin-specific Fab, glucagon, calcium, inotropic medications, and vasopressors, remain the mainstay in the treatment of drug-induced dysrhythmias. Given the lack of success of pacing, possible downsides, and the greater effectiveness of specific antidotes, it is not standard to routinely attempt transvenous cardiac pacing in the setting of drug overdose. However, as a last resort, cardiac pacing can be supported.

Contraindications

The presence of a prosthetic tricuspid valve is generally considered to be an absolute contraindication to transvenous cardiac pacing. In addition, severe hypothermia will occasionally result in ventricular fibrillation when pacing is attempted. Because ventricular fibrillation under these conditions is difficult to convert, caution is advised when considering pacing severely hypothermic and bradycardic patients. Rapid and careful rewarming is often recommended first, followed by pacing if the patient's condition does not improve.

Equipment

Several items are required to insert a transvenous pacemaker adequately. Like most special procedures, a prearranged tray is convenient. The usual components required to insert a transvenous cardiac pacemaker are depicted in Review Box 15.1 .

Pacing Generator

Many different pacing generators are available, but in general they all have the same basic features. The controls will frequently have a locking feature or cover to prevent the generator from being switched off or reprogrammed inadvertently. An amperage control allows the operator to vary the amount of electrical current delivered to the myocardium, usually 0.1 to 20 mA. Increasing the setting increases the output and improves the likelihood of capture. The pacing control mode is determined by adjusting the gain setting for the sensing function of the generator. By increasing the sensitivity, one can convert the unit from a fixed-rate (asynchronous mode) to a demand (synchronous mode) pacemaker. The typical pacing generator has a sensitivity setting that ranges from approximately 0.5 to 20 mV. The voltage setting represents the minimum strength of the electrical signal that the pacer is able to detect. Decreasing the setting increases the sensitivity and improves the likelihood of sensing myocardial depolarization. In the fixed-rate mode, the unit fires despite the underlying intrinsic rhythm; that is, the unit does not sense any intrinsic electrical activity. In the full-demand mode, however, the pacemaker senses the underlying ventricular depolarizations, and the unit does not fire as long as the patient's ventricular rate is equal to or faster than the set rate of the pacing generator. A sensing indicator meter and a rate control knob are also present.

Temporary pacing generators are battery operated, and thus it is always good practice to install a fresh battery whenever pacing is anticipated. An example of a pacing generator is shown in Fig. 15.1 .

Figure 15.1, Pacemaker energy source: controls and connections.

Pacing Catheters and Electrodes

Several sizes and brands of pacing catheters are available. In general, most range from 3 to 5 Fr in size and are approximately 100 cm in length. Lines are marked along the catheter surface at approximately 10-cm intervals and can be used to estimate catheter position during insertion. Pacing catheters differ with respect to their stiffness, electrode configurations, floating characteristics, and other qualities. For emergency pacing, the semifloating bipolar electrode catheter with a balloon tip is used most frequently ( Fig. 15.2 ). The balloon holds approximately 1.5 mL of air, and the air injection port has a locking lever to secure balloon expansion. Before insertion, check the balloon for leakage of air by inflating and immersing it in sterile water. The presence of an air leak is noted by a stream of bubbles rising to the surface of the water. An inflated balloon helps the catheter “float” into the heart, even in low-flow states, but is not advantageous in the cardiac arrest situation.

Figure 15.2, Balloon-tipped pacing catheter.

For all practical purposes, temporary transvenous pacing is accomplished with a bipolar pacing catheter. The terms unipolar and bipolar refer to the number of electrodes in contact with the portion of the heart that is to be stimulated. All pacemaker systems must have both a positive (anode) and a negative (cathode) electrode; hence, all stimulation is bipolar. In the typical bipolar catheter used for temporary transvenous pacing, the cathode (stimulating electrode) is at the tip of the pacing catheter. The anode is located 1 to 2 cm proximal to the tip, and a balloon or an insulated wire separates the two electrodes. The distinction between unipolar and bipolar pacing catheters is that a bipolar catheter has both electrodes in relatively close proximity on the catheter and both may contact the endocardium. In a bipolar catheter, the electrodes are usually stainless steel or platinum rings that encircle the pacing catheter. When properly positioned, both electrodes will be within the right ventricle so that a field of electrical excitation is set up between the electrodes. With a bipolar catheter, the cathode does not need to be in direct contact with the endocardium for pacing to occur, although it is preferable to have direct contact.

A unipolar system is also effective but is used infrequently for temporary transvenous pacing. In a unipolar system, the cathode is at the tip of the pacing catheter and the anode is located in one of three places: in the pacing generator itself, more proximally on the catheter (outside the ventricle), or on the patient's chest. A bipolar system may be converted to a unipolar system by simply disconnecting the positive proximal connection of the bipolar catheter from the pacing generator and running a new wire from the positive (pacing generator) terminal to the patient's chest wall. Such a conversion may be required in the unlikely event of failure of one lead of the bipolar system.

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