Chapter 14 / Pacing During Cardiac Arrest

14

245

Pacing During Cardiac Arrest

Allan S. Jaffe, MD and Utpal H. Pandya, MD
CONTENTS
INTRODUCTION
APPROACH TO TREATMENT
REFERENCES

INTRODUCTION
The incidence of sudden arrhythmic deaths continues to be a significant problem
despite the fact that mortality from acute coronary syndromes continues to decrease in
response to early interventions and improved secondary prevention (13). Most patients
with coronary artery disease who suffer cardiac arrest (CA) do not have acute myocardial
infarction (AMI [46]). Thus, primary arrhythmic causes of CA are becoming increasingly important.
An estimated 400,000 to 460,000 people suffer CA annually. The initial rhythm noted
in earlier studies was predominantly ventricular fibrillation (VF) in up to 75% of cases,
with asystole at 20% and pulseless electrical activity (PEA) accounting for 5% (1,4,6).
Survival was directly related to the initial rhythm. Patients with VF had a 25% survival,
whereas when the arrest rhythm was asystole, it was only 1%. The likelihood of the
rhythm being asystole increased proportionately as the time from collapse to resuscitation increased.
Bayes de Deluna (7) found that the initial rhythm was frequently ventricular tachycardia (VT), which degenerated into VF (62% of cases) in a study of 157 patients with CA
whose event occurred as they were being evaluated with ambulatory electrocardiographic
monitoring. Bradycardia was the primary initial rhythm in only 17%. With the advent of
first responder-initiated defibrillation, the success rate of resuscitation in patients with
VF or VT is improving (4,9). Yet, the rates of survival in asystole and/or PEA continue
to be dismal (9).
Unfortunately, with implantable cardioverter defibrillators and modern therapy, the
percentage of patients with VT/VF as an initial rhythm is declining. In the most recent
tabulation by Cobb and colleagues (10), the annual incidence of CA as a result of VF had
declined by approx 56% despite improved response times in most emergency medical
systems. At present, VF as a first rhythm may occur in less than 50% of patients (10). In
Seattle at least, asystole as an initial arrest rhythm seems to increasing in women but not
in men.
From: Contemporary Cardiology: Cardiopulmonary Resuscitation
Edited by: J. P. Ornato and M. A. Peberdy Humana Press Inc., Totowa, NJ

245

246

Cardiopulmonary Resuscitation
Table 1
Common Causes of Bradysystolic Arrest
Drugs
`-Blockers
Diltiazem/verapamil
Digoxin
Clonidine
Class IA, IC, and III antiarrhythmics
Autonomic
Increased vagal output
Vasodepressor reflex
Carotid hypersensitivity
Hyperkalemia
Acute myocardial infarction
Right Coronary Territory (more likely)
Hypothyroidism
Hypothermia
Sepsis
Infectionendocarditis, atrioventricular block in Lyme
disease

APPROACH TO TREATMENT
An initial rhythm of asystole has been thought to be a sign of a delay from collapse to
recognition/resuscitation or a clue to the presence of a failing heart with local acidosis that
precludes effective electrical-mechanical coupling. However, in some circumstances,
there are reversible causes of bradyasystole (Table 1). If one can identify and treat these
causes early the odds of survival may increase by preventing the initial bradyarrhythmias
from disintegrating into asystole.
One of the most obvious reversible causes is AMI/myocarial ischemia with heart
block. Treatment of the underlying ischemia usually reverses the bradycardia, which is
often vagally mediated and may respond to atropine if the right coronary artery is involved.
If the left system and particularly the left anterior descending territory is problematic, then
the mechanism of bradycardia is more apt to be Mobitz Type 2 second degree atrioventricular block or complete heart block with a wide QRS escape rhythm, which requires
urgent pacing. Mechanical causes such as ventricular rupture, cardiac tamponade, large
pulmonary emboli, and tension pneumothorax also respond to relief of the underlying
abnormality.
These observations suggest that the phases of resuscitation recently proposed by
Weisfeld and Becker (11) may be helpful with bradyasystolic rhythms as well as VF.
Weisfeld and Becker define an initial period in which they recommend electrical therapy,
a period in which circulatory support is needed, and finally a metabolic phase. For
bradycardia, there should be an initial phase prior to asystole in which the aggressive use
of pacing and pharmacological therapy may be helpful, a second phase in which correctable abnormalities should be sought as circulatory assistance is being provided and
finally a metabolic phase.

Chapter 14 / Pacing During Cardiac Arrest

247

Specific Etiologies Considered During the Early Phase

A large variety of cardiac abnormalities can lead to bradycardia (Table 1). The longstanding experience with external pacemakers suggest that results are excellent when one
uses the device acutely but prior to bradyasystolic arrest. The most common situation is
when there is acute ischemic heart disease accompanied by drug toxicity with or without
electrolyte imbalance, intrinsic conducting system disease, operative trauma (coronary
artery bypass graft and or ablation), and/or acute vagal insults such as an acute intraabdominal catastrophe. Although there are no randomized controlled trials, the most
important clinical rule is that early initiation of pacing, before asystole, is the key to a
good outcome. Coincident with the initiation of pacing, a thorough search for potential
etiologies is mandated.
Mnemonics exist to make it facile for the physician to consider the essential diagnostic
considerations in patients who present with pulseless electric activity. One mnemonic
that has become popular is the five Hs and Ts. They are also usually appropriate for
patients who present with asystole. The five Hs are hypoxia, heart attack, hypovolemia,
H+ (electrolyte abnormality), and hypothermia. If one thinks of hypovolemia as an acute
process (e.g., cardiac or aortic rupture), although not common, this mnemonic works for
bradycardia as well. The five Ts are to test for other pulses, tension pneumothorax,
tamponade, toxins and therapeutic agents, and thrombo-emboli (12).

Correctable Abnormalities As Circulatory Support Is Provided

Once asystole is present, the prognosis is grim. In addition to attempting to find
remediable causes, pacing is worth an attempt.

The Metabolic Phase

Early intervention is critical because a variety of metabolic abnormalities develop
when there is persistent and/or progressive hypoperfusion. With reduced oxygen delivery, metabolism shifts from aerobic to anaerobic pathways. Even with the subsequent
initiation of cardiopulmonary resuscitation (CPR), only approx 25% of the cardiac output
is restored. Because of the reduction in cardiac output and subsequent decrease in critical
organ system and coronary blood flow, tissue hypoxia ensues. This leads to anaerobic
metabolism and the accumulation of hydrogen ions. Acid residues are buffered by endogenous buffers, usually bicarbonate, which leads to the production of carbon dioxide.
Carbon dioxide diffuses across the cell membrane and leads to tissue acidosis and cellular
dysfunction, which is reflected in the venous circulation. Additionally, acidosis leads to
competition for calcium ions binding to troponin. This inhibits the cross bridging between
actin and mycin filaments and, hence, myocardial contractility. Hyperventilation during
CPR removes the excess CO2 but does not reverse the tissue acidosis as a result of the
reduced delivery of blood back to the heart. Thus, there is an arteriovenous paradox
(13,14) with hypercarbic venous acidemia and hypocarbic arterial alkalemia.
This is also the reason why bicarbonate is not helpful. It buffers arterial acidosis, but
the increased CO2 produced exacerbates venous and tissue acidosis. This local tissue
acidosis, which is common in patients presenting with asystole whose time from collapse
to resuscitation is often prolonged, is why pacing has little chance of success if applied
too late (see Table 2). Moreover bicarbonate may have adverse effects such as depression
of myocardial function, inactivation of catecholamines, and paradoxical central nervous
system acidosis.. It may be that with time and better techniques to enhance blood flow
in the future, local tissue acidosis may be obviated but we are not at that point presently.

248

Prehospital

Prehospital

Eitel (1987; 26)

Syverud (1986; 19)

Prehospital

Barthell (1988; 28)

Prehospital

Prehospital

Cummins (1993; 29)

Vukov (1988; 27)

Venue pacing
initiated

Primary investigator
(year; reference)

19 patients: 9 with asystole,

9 with PEA
Group 1: 4/19 pacing within
5 minutes.
Group 2: Pacing 520 minutes

91 paced (59 asystole, 32 PEA;

44/59 primary asystole)

58 patients (33 primary and 25 postshock asystole). No controls.

103 paced for primary asystole

and EMD and secondary asystole
EMD 136 controls

112 patients with primary asystole;

46 patients with postdefibrillation
asystole; a control group of 259

Patient population

2/5 in group 1 with neurologic

recovery, none in group 2

85/91(93%) electrical capture

10/91 (11%) mechanical capture
1 patient admitted,
0 survived to discharge

4/58 patients admitted to hospital,

none suvived at day

No statistically significant
difference in outcome for
pacing in EMD or asystole
whether 1 or 2

No statistically significant
advantage in intervention group
for hospital admission
or survival outcomes.
Technically feasible.

Results

Table 2
Trials of Pacing for Asystole

Cardiopulmonary Resuscitation
Emphasizes the role of early pacing

69/91 patients pharmacologic

intervention prior to pacing
(epinephrine, atropine,
bicarbonate) no difference
in resuscitation

Rural setting, with very high CA

resuscitation rates. 32% paced
within 10 minutes of collapse

5/6 patients with hemodynamically

significant bradycardias
survived with pacing

Pacing not occasionally initiated

in the field as a result of EMT
training schedule and negative
No difference between primary
or postshock asystole

Comments

248

249

In-hospital

ED

Dalsey (1984; 22)

Zoll (1956; 23)

In-hospital

Noe (1985; 24)

Prehospital

Prehospital

Paris (1985; 25)

Jaggaroa (1982; 20)

Prehospital

Hedges (1987; 21)

25/34 patients with Stokes-Adams

attacks

25 patients (16 late and 9 early arrest)

Included 1 or 2 asystole/PEA

52 unconscious patients ( 30 asystole,

22 PEA)

TCP in 23/24 patients for asystole

TVP in 4/23 patients of asystole

112 patients (55 asystole, 44 PEA)

101(89 actually paced) pacing group;

101 control group
28/101 pacing group with primary
asystole
45/101 VT/VF degenerating into
paceable rhythm

Mechanical capture with longterm survivors in the 25 with

ventricular standstill

Late group no survivors

Early group 3 survivors

50% with electrical capture,

15% mechanical capture.
No survivors

Two of 24 patients with

TCP survived

52% electrical capture,

8% mechanical capture.
No survivors to discharge

Average time from arrest to

pacing: 21.8 minutes
Outcome measures not
statistically significant
between groups

Prompt use of device after rhythm

noted

2/3 survivors were postdefibrillation asystole. No

survivors in primary asystole

Most paced after 20 minutes of

arrest.
Pacing attempted after failed
drug therapy

The two survivors were

conscious with the arrest and
had very early intervention

Average time from arrest to

pacing was 29 minutes
Pharmacologic interventions
implemented prior to pacing

Neurologically intact patient

excluded. (When paced
did well)
Initial rhythm of VT/VF and
short time to ACLS
favorable outcome

Chapter 14 / Pacing During Cardiac Arrest

249

250

Cardiopulmonary Resuscitation

Pacing Techniques
HISTORICAL PERSPECTIVE
In 1791, Galvani was the first to note that an electrical current applied across a frog
heart could lead to myocardial contraction. Hyman and others in the early 1930s reported
that animals who were asystolic as a result of anoxia had restoration of a perfusing rhythm
after being subjected to pulsating current (14). The first report of the application of
transcutaneous pacing in humans was by Paul Zoll (15). He applied the technique to two
patients with Stokes Adams attacks (ventricular standstill) in an attempt to restore a
rhythm. He used two subcutaneous external needles to deliver electrical energy across the
chest wall. One patient died after 20 minutes of external pacing from cardiac tamponade
as a result of previously applied intracardiac injections. The second patient survived after
having been paced externally for 5 days when he developed a perfusing intrinsic
idioventricular rhythm. Prior to this demonstration of the feasibility of the technique,
intravenous or intracardiac epinephrine myocardial stimulation with direct massage or
needles had been attempted to reverse asystolic CA with only limited success and incremental risks.
Zoll later refined the transcutaneous pacing technique with the introduction of a pair
of 3-cm metal electrodes, which were designed to deliver 2-ms, 120-volt AC impulses.
However, the 2-ms pulse durations resembled a short action potential of skeletal muscle
rather than the longer action potentials of myocardial tissue, which led to preferential
stimulation of skeletal muscle and discomfort. Also, the shorter pulse width required
higher current (amperage) to reach stimulation thresholds. Finally, a smaller sized electrode meant that the current density was very high at the electrodeskin interface leading
to cutaneous pain in the conscious patient. Transcutaneous pacemakers fell into disuse
somewhat with the advent of implantable transvenous pacemakers. In the early 1980s,
transcutaneous pacemaker and electrode pad improvements made this technique much
more effective and better tolerated by patients. By increasing the pulse duration to 20
to 40 milliseconds and increasing the size of the electrodes (from 3 cm to 8 cm) to 50
to 100 cm (2), the painful side effects of transcutaneous pacing were reduced, allowing
the use of the technique in emergency situations.
Before transcutaneous pacemaking became safe and effective, temporary transvenous
cardiac pacing was attempted in the majority of urgent circumstance. Balloon-tipped,
transvenous pacing catheters are safe and expeditious and can be placed rapidly in the
emergent setting by experienced operators (16). However, it is clear that transcutaneous
pacing seems to be both easier and more efficacious in the majority of current clinical
settings.

Specific Techniques
TRANSCUTANEOUS PACING
Transcutaneous pacing is remarkably easy to apply. Two pads are applied. The larger
(ground) electrode is applied posteriorly in the midline between the mid-scapula and T4
vertebra. The anterior electrode is best applied at the electrocardiographic V3 position.
When possible, body hair should be removed, but it is not recommended that it be
shaved prior to electrode placement. The nicks caused by shaving have been reported
to cause uneven conduction and, therefore, burns through areas of lesser resistance.
Once the electrodes are applied and the pacer cable connected to its output source, one
sets the generator rate to 20 to 30 beats per minute over the patients spontaneous rate.

Chapter 14 / Pacing During Cardiac Arrest

251

In general, the output is set initially at 50 milliamps. If the pacemaker does not capture,
then the output is increased progressively to a maximum (usually 200 milliamps) or
until capture. Once capture is achieved, one should reduce the output until capture is
lost. This is called the stimulation threshold. Subsequently, one sets the output at 20%
above the stimulation threshold.

Temporary Transvenous Pacing

A balloon tip, Swan pacing catheter is often used in an emergency situation because
it obviates the need for fluoroscopy, which is difficult at best in the urgent circumstance. The procedure begins with gaining access percutaneously via the subclavian or
internal jugular vein using the Seldinger technique. Subsequently, the distal pole of the
electrode is connected to the chest lead of the electrocardiogram (ECG). Next, the
balloon is inflated and the catheter electrode is advanced with monitoring of the intracavitary ECG. Once typical intraventricluar electrocardiographic complexes appear,
the balloon is deflated to prevent flotation in the pulmonary artery. If a balloon tip Swan
pacing catheter is used, the location of catheter can be deduced from the pressure
tracings. Large ventricular ECGs showing an injury current (ST elevation) signal contact with the endothelium.
The effect of acute interventions after asystole is established have been disappointing
(17,18). Efficacy is better for potentially presaging rhythms, like heart block (see above).
The initial nonrandomized small pacing study by Jaggarao (19) in 1982 in the prehospital
setting showed some promise. There were three survivors out of nine patients with
asystole or PEA who had early pacing. Two of the survivors were asystolic postdefibrillation. Hedges defined an early period of 5 minutes or less of asystolic CA as an important factor that correlated with successful resuscitation (20). Often, he was dealing with
rhythms the presaged asystole rather than asystole itself. Studies by Dalsey et al. (21)
have shown that transcutaneous pacing is just as effective in the setting of CA in capturing the myocardium.
Lessons from these early studies laid the groundwork for the randomized trials in the
late 1980s and 1990s. The portability of transcutaneous pacing made it possible for
paramedics to use the technique in the field. Trials were designed to pace the patient in
the prehospital setting, even prior to traditional pharmacologic interventions in some
cases. However, without exception, these studies have been resoundingly negative once
asystole has been established (Table 2). This is why early initiation of definitive therapy
with either atropine, isoproterenol, or pacing prior to the onset of asystolic arrest and,
subsequently, an aggressive source for underlying abnormalities is so critical.

REFERENCES
1. Myerburg RJ, Kessler KM, Castellanos A. Sudden cardiac death: epidemiology, transient risk, and
intervention assessment. Ann Intern Med 1993; 119:118797.
2. Myerburg RJ, Interian A Jr, Mitrani RM, Kessler KM, Castellanos A. Frequency of sudden cardiac death
and profiles of risk. Am J Cardiol 1997; 80:10F19F.
3. Gordon T, Thom T. The recent decrease in CHD mortality. Prev Med 1975; 4:115125
4. Cobb LA, Werner JA, Trobaugh GB. Sudden cardiac death: I. A decades experience with out-ofhospital resuscitation. Mod Concepts Cardiovasc Dis 1980; 49:3136
5. Cobb LA, Werner JA, Trobaugh GB. Sudden cardiac death: II. Outcome of resuscitation, management,
and future directions. Mod Concepts Cardiovasc Dis 1980; 49:3742
6. Cobb LA, Baum RS, Alvarez H III, Schaffer WA. Resuscitation from out-of-hospital ventricular fibrillation: 4 years follow-up. Circulation 1975; 51:III-223III-228

252

Cardiopulmonary Resuscitation

7. de Luna AB, Coumel P, Leclercq JF. Ambulatory sudden cardiac death: mechanisms of production of
fatal arrhythmias on the basis of data from 157 cases. Am Heart J 1989; 117:151159
8. Thompson RG, Hallstrom AP, Cobb LA. Bystander-initiated CPR in management of ventricular fibrillation. Ann Intern Med 1979; 90:737740.
9. Greene HL: Sudden Arrhythmic Cardiac DeathMechanisms, Resuscitation and Classification: The
Seattle Perspective. Am J Cardiol 1990; 65:4B12B
10. Cobb LA, Fahrenbruch CE, Olsufka M, Copass M. Changing Incidence of Out-of-Hospital Ventricular
Fibrillation, 19802000. JAMA 2002; 288:30083013.
11. Weisfeldt ML, Becker LB. Resuscitation after cardiac arrest-A 3-phase time-sensitive model. JAMA
2002; 288:30353038.
12. Grundler WG, Weil Mh, Rackow EC. Arteriovenous carbon dioxide and pH gradients during cardiac
arrest. Circulation 1982; 66:297302
13. Jaffe, AS: Cardiovascular Pharmacology I. Circulation 1986; 74S:IV-70IV-73.
14. Weil MH, Rackow EC, Trevino R, et al. Difference in acid-base state between venous and arterial blood
during cardiopulmonary resuscitation. N Engl J Med 1986; 315:153156.
15. Hyman AS. Resuscitation of the stopped heart by intracardial therapy. Arch Int Med 1932; 50:283.
16. Zoll P. Resuscitation of the heart in ventricular standstill by external electric stimulation. N Eng J Med
1952; 247:768771.
17. Lang R, David D, Klein HO, et al. The use of the balloon-tipped floating catheter in temporary trasvenous
cardiac pacing. PACE 1981; 4:491496.
18. Zoll PM, Zoll RH, Falk RH, Clinton JE, Eitel DR, Antman EM. External noninvasive temporary cardiac
pacing: clinical trials. Circulation 1985; 71:937.
19. Syverud SA, Dalsey WC, Hedges JR. Transcutaneous and transvenous cardiac pacing for early
bradysystolic cardiac arrest. Ann Emerg Med 1986; 15:121.
20. Jaggarao NSV, Heber M, Grainger R, et al. Use of an automated external defibrillator-pacemaker by
ambulance staff. Lancet 1982; 2:7375.
21. Hedges JR, Syverud SA, Dalsey WC, Feero S, Easter R, Shultz B. Prehospital trial of emergency
transcutaneous cardiac pacing. Circulation 1987; 76:13371343.
22. Dalsey WC, Syverud SA, Hedges JR. Emergency department use of transcutaneous pacing for cardiac
arrests. Crit Care Med 1985; 13:399401.
23. Zoll PM, Linenthal AJ, Norman LR. External electric stimulation of the heart in cardiac arrest. Arch
Intern Med 1956; 96:639653.
24. Noe R, Cockrell W, Moses HW, Dove IT, Batchelder JE. Transcutaneous pacemaker use in a large
hospital. PACE 1986; 9:101104.
25. Paris PM, Stewart RD, Kaplan RM, Whipkey R. Transcutaneous pacing for bradyasystolic cardiac
arrests in prehospital care. Ann Emerg Med 1985; 14:320323.
26. Eitel DR, Guzzardi LJ, Stein SE, Drawbaugh RE, Hess DR, Walton SL. Non invasive transcutaneous
cardiac pacing in prehospital cardiac arrests. Ann Emerg Med 1987; 16 531534.
27. Vukov LF, White RD, Bachman JW, OBrien PC. New perspectives on rural EMT defibrillation. Ann
Emerg Med 1988; 17:318321.
28. Barthell E, Troiano P, Olson D, Stueven HA, Hendley G. Prehospital external cardiac pacing: a prospective, controlled clinical trial. Ann Emerg Med 1988; 17:12211226.
29. Cummins RO, Graves JR, Larsen MP, Hallstrom AP, Hearne TR, Ciliberti J, Nicola RM, Horan S. Outof-hospital transcutaneous pacing by emergency medical technicians in patients with asystolic cardiac
arrest. N Engl J Med. 1993; 328:13771382.