Emergency Cardiac Pacing

Edward S. Bessman

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 has been used for this condition. Several approaches to pacing can be taken, including transcutaneous, transvenous, transthoracic, epicardial, endocardial, and esophageal. Transcutaneous and transvenous 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 emergency cardiac pacemakers, many have mastered the techniques and are often the only clinicians available to perform this lifesaving procedure.

Emergency Transvenous Cardiac Pacing

Review Box 15-1 Transvenous cardiac pacing: indications, contraindications, complications, and equipment.

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.¹ 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.²

However, 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.

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.³

Furman and Robinson demonstrated the transvenous endocardial approach in humans in 1958.⁴ 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.⁵ 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.⁶ One year later, Kimball and Killip used this technique to insert endocardial pacemakers at the bedside.⁷ 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.⁸

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.⁹ 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

Rosenberg and coworkers introduced an improved pacing catheter known as the Elecath semifloating pacing wire.¹ The Elecath was stiffer than the Flexon steel wire electrode that was in prevailing use. Rosenberg and coworkers¹ 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.¹⁰ Schnitzler and colleagues successfully used this method for placement of a right ventricular pacemaker in 15 of 17 patients.¹¹

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.¹² 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 (Table 15-2).

TABLE 15-2

History of Transvenous Pacing

DATE	INVESTIGATOR	EVENT
1700	Early investigators	First restimulation studies
1951	Callaghan and Bigelow	First transvenous approach in dogs
1952	Zoll	Transcutaneous cardiac stimulator
1958	Falkmann and Walkins	Implanted pacing wires after surgery
1959	Furman and Robinson	First transvenous pacer in humans
1964	Vogel et al.	Flexible electrocardiographic catheter without fluoroscopy
1965	Kimball and Killip	First bedside transvenous pacing
1966	Goetz et al.	Demand pacemaker developed
1967	Zuckerman et al.	Use of a demand pacemaker clinically
1969	Rosenberg et al.	Semifloating pacing catheter
1973	Schnitzler et al.	Balloon-tipped pacers

Birkhahn and coworkers retrospectively compared the experience of emergency physicians with that of cardiologists in placing transvenous pacemakers under ECG guidance.¹³ 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.

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.¹⁴ 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.¹⁵ 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.¹⁶ 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.¹⁷ Transvenous pacing alone may also not be effective for post-countershock pulseless bradyarrhythmias.¹⁸ 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.¹⁷ 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 achieved¹⁹ (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.²⁰

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.²¹

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%.²² First-degree block progresses to second- or third-degree block 33% of the time, and second-degree block progresses to third-degree block about one third of the time.²³

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.²⁴

Hypovolemia and hypotension can cause ischemia of conduction tissue and cardiac dysfunction.²⁵ Marked bradyarrhythmias that persist even after vigorous volume replacement may rarely respond to cardiac pacing in patients with such trauma.²⁶

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 uncomplicated infarction. Atkins and colleagues noted that 18% of patients with MI had bundle branch block.²⁷ 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.²⁸ 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 15-3).

TABLE 15-3

Influence of Different Variables on the Risk for High-Degree AVB in Patients with BBB during MI

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; MI, myocardial infarction; RBBB, right bundle branch block.

From American Heart Association 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. 1978;58:690.

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.²⁸ Though controversial, one authority recommends prophylactic pacing for all new bundle branch blocks when MI is evident.²⁹

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.³⁰ 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.³¹ 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.³² 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.³³

One final point to bear in mind regarding bradydysrythmias in the setting of AMI is that most of the studies investigating temporary pacing were done in the era before the use of thrombolytic agents or percutaneous coronary angioplasty. Modern treatment of AMI is substantially different, but more recent studies, particularly those involving prophylactic pacing, are lacking.

Tachycardias

Hemodynamically compromising tachycardias are usually treated by medical means 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.³⁴ Overdrive pacing is especially useful for arrhythmias with recurrent prolonged QT intervals such as those seen with quinidine toxicity or torsades de pointes.³⁵ 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.³⁶

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 case reports of success.37–40 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.⁴¹

Contraindications

The presence of a prosthetic tricuspid valve is generally considered to be an absolute contraindication to transvenous cardiac pacing.⁴² Also, 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 bradycardiac patients. Rapid and careful rewarming is often recommended first, followed by pacing if the patient’s condition does not improve.

The ECG machine should be placed in a manner that allows easy visibility of the rhythm during insertion. One method is to place the machine near the level of the patient’s midthorax facing the operator, on either side of the patient as logistics and operator preference allow (Fig. 15-3). Note that the operator stands at the head of the patient during passage of the catheter through the internal jugular or subclavian vein and at the midabdomen for insertion through the femoral or brachiocephalic vein. Newer patient monitors may be equipped with suitable ECG connections to allow their use in place of a stand-alone ECG machine. Because these patients will already be attached to a monitor, it may prove convenient to use the same piece of equipment to assist in insertion of the pacemaker.

Figure 15-3 Position of an electrocardiographic device during insertion of a pacemaker catheter through the left subclavian vein.

Introducer Sheath

An introducer set or sheath is required for venous access (see Chapter 22). Some pacing catheters are prepackaged with the appropriate equipment, whereas others require a separate set. The introducer set is used to enhance passage of the pacing catheter through the skin, subcutaneous tissue, and vessel wall. The sheath must be larger than the pacing catheter to allow it to pass. The size of the pacing catheter refers to its outside diameter, whereas the size of the introducer refers to its inside diameter. Thus, a 5-Fr pacing catheter will fit through a 5-Fr introducer. Introducer sheaths are available with a perforated elastic seal covering the opening through which the pacing catheter is passed (pacer port). The seal allows the catheter to be manipulated while preventing blood from escaping or air from entering the vein. A side port allows the sheath to be used for central venous access. A makeshift sheath can be fashioned with an appropriately sized intravenous (IV) catheter. For a 3-Fr balloon-tipped catheter, a 14-gauge 1.5- to 2-inch IV catheter is suitable. A 4-Fr balloon-tipped catheter will also fit through a 14-gauge catheter or needle. However, without a seal over the hub, blood will leak from the end of the IV catheter.

Overall, the key to success with this procedure is preparation. In a typical ED there are often a variety of vascular access kits and devices, not all of which will work well, if at all, for passing a pacing catheter. It is imperative that one examine all the components of the tray before starting the procedure to ensure that all wires, sheaths, dilators, and syringes fit as expected. Ideally, all the equipment and accessories needed for emergency pacemaker insertion should be kept together in a designated location.

Procedure

A checklist for the preparation and initial setup of a pacing generator is shown in Box 15-1. It may be useful to have a copy of this checklist or a similar list stored with the pacemaker to have on hand in emergency situations.

Box 15-1 Checklist for a Temporary Transvenous Pacing Generator *

• Insert a new battery.

• Turn the pacemaker ON.

• Set the RATE (80 beats/min), OUTPUT (5 mA), and SENSITIVITY (3 mV).^†

• Connect the patient cable to the pacemaker.

• Open both connector terminals on the patient cable.

• Insert the PROXIMAL (+) pin of the pacing catheter into the POSITIVE (+) connector terminal on the patient cable.

• Tighten the connection firmly.

• Use alligator clips to connect the DISTAL (−) pin of the pacing catheter to lead V₁ of electrocardiographic machine.

• When the catheter is in position, remove the DISTAL (−) pin from V₁ and insert it into the NEGATIVE (−) connector terminal on the patient cable.

• Tighten the connection firmly.

^*Adjust pacemaker settings as needed to achieve proper capture and sensitivity (see text).

^†Guidelines only. Follow the recommendations of the device’s manufacturer if different.

Patient Preparation

Patient instruction is an extremely important aspect of any procedure. Frequently, there is not enough time to give patients a detailed explanation or to obtain written informed consent. Nonetheless, sufficient information should be provided so that the patient feels at ease. It is always prudent to obtain and document informed consent from the patient, if possible, before any invasive procedure or to document that the circumstances did not allow informed consent. Patients should be assured that they will feel no discomfort after the venipuncture site has been anesthetized and that they will feel better when the catheter is in place and is functional. Continued reassurance is required during the procedure because patients are usually facing away from the operator and their faces are often covered; thus they may be unsure of what is occurring. Sedation and analgesia should be considered when appropriate.

All operators should wear surgical masks, caps, gloves, and gowns to decrease the risk for infection before catheter placement. Patients should be prepared and draped in the usual sterile fashion. This aseptic precaution should also be explained to the patient.

Site Selection

The four venous channels that provide easy access to the right ventricle are the brachial, subclavian, femoral, and internal jugular veins (Table 15-4). The route selected is often one of personal or institutional preference. The right internal jugular and left subclavian veins have the straightest anatomic pathway to the right ventricle and are generally preferred for temporary transvenous pacing (Fig. 15-4). In some centers a particular site is preferred for permanent transvenous pacemaker placement, and if possible, this site should be avoided for temporary placement.

TABLE 15-4

Advantages and Disadvantages of Pacemaker Placement Sites

VENOUS CHANNELS	ADVANTAGES	DISADVANTAGES
Brachial	Very safe route Vessel easily accessible, either by cutdown or a percutaneous approach Compressible	Often requires a cutdown Easily displaced and poor patient mobility Not reusable if a cutdown technique is performed The catheter is more difficult to advance than in central or larger vessels
Subclavian	Direct access to the right side of the heart (especially via the left subclavian) Rapid insertion time Good patient mobility	Pneumothorax and other intrathoracic trauma are possible Noncompressible
Femoral	Direct access to the right side of the heart Rapid insertion time Compressible	Increased incidence of thrombophlebitis Can be dislodged by leg movement Poor patient mobility Infection
Internal jugular	Direct access to the right side of the heart (especially via the right internal jugular) Rapid insertion time Compressible	Possible carotid artery puncture Dislodgment with movement of the head Thrombophlebitis