14 Pacing During Cardiac Arrest

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From: Contemporary Cardiology: Cardiopulmonary Resuscitation Edited by: J. P. Ornato and M. A. Peberdy © Humana Press Inc., Totowa, NJ

14 Pacing During Cardiac Arrest

Allan S. Jaffe, ^MD and Utpal H. Pandya, ^MD

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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 (1–3). Most patients with coronary artery disease who suffer cardiac arrest (CA) do not have acute myocardial infarction (AMI [4–6]). Thus, primary arrhythmic causes of CA are becoming increas- ingly 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 resuscita- tion increased.

Bayes de Deluna (7) found that the initial rhythm was frequently ventricular tachycar- dia (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.

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 atrioven- tricular 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 correct- able abnormalities should be sought as circulatory assistance is being provided and finally a metabolic phase.

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

Infection—endocarditis, atrioventricular block in Lyme disease

Specific Etiologies Considered During the Early Phase

A large variety of cardiac abnormalities can lead to bradycardia (Table 1). The long- standing 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 intra- abdominal 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 deliv- ery, 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 endog- enous 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 CO

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 CO

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.

Table 2 Trials of Pacing for Asystole Primary investigatorVenue pacing (year; reference)initiatedPatient populationResultsComments Cummins (1993; 29)Prehospital112 patients with primary asystole;No statistically significantPacing not occasionally initiated 46 patients with postdefibrillationadvantage in intervention groupin the field as a result of EMT asystole; a control group of 259for hospital admissiontraining schedule and negative or survival outcomes.No difference between primary Technically feasible.or postshock asystole Barthell (1988; 28)Prehospital103 paced for primary asystoleNo statistically significant5/6 patients with hemodynamically and EMD and secondary asystoledifference in outcome forsignificant bradycardias EMD 136 controlspacing in EMD or asystole survived with pacing whether 1° or 2° Vukov (1988; 27)Prehospital58 patients (33 primary and 25 post-4/58 patients admitted to hospital,Rural setting, with very high CA shock asystole). No controls.none suvived at dayresuscitation rates. 32% paced within 10 minutes of collapse Eitel (1987; 26)Prehospital91 paced (59 asystole, 32 PEA;85/91(93%) electrical capture69/91 patients pharmacologic 44/59 primary asystole)10/91 (11%) mechanical captureintervention prior to pacing 1 patient admitted,(epinephrine, atropine, 0 survived to dischargebicarbonate)‚ no difference in resuscitation Syverud (1986; 19)Prehospital19 patients: 9 with asystole,2/5 in group 1 with neurologicEmphasizes the role of early pacing 9 with PEArecovery, none in group 2 Group 1: 4/19 pacing within 5 minutes. Group 2: Pacing 5–20 minutes

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Hedges (1987; 21)Prehospital101(89 actually paced) pacing group;Average time from arrest toNeurologically intact patient 101 control grouppacing: 21.8 minutesexcluded. (When paced 28/101 pacing group with primaryOutcome measures notdid well) asystolestatistically significantInitial rhythm of VT/VF and 45/101 VT/VF degenerating intobetween groupsshort time to ACLS paceable rhythmfavorable outcome Paris (1985; 25)Prehospital112 patients (55 asystole, 44 PEA)52% electrical capture,Average time from arrest to 8% mechanical capture.pacing was 29 minutes No survivors to dischargePharmacologic interventions implemented prior to pacing Noe (1985; 24)In-hospitalTCP in 23/24 patients for asystoleTwo of 24 patients withThe two survivors were TVP in 4/23 patients of asystoleTCP survivedconscious with the arrest and had very early intervention Dalsey (1984; 22)ED52 unconscious patients ( 30 asystole,50% with electrical capture,Most paced after 20 minutes of 22 PEA)15% mechanical capture.arrest. No survivorsPacing attempted after failed drug therapy Jaggaroa (1982; 20)Prehospital25 patients (16 late and 9 early arrest)Late group no survivors2/3 survivors were post- Included 1° or 2° asystole/PEAEarly group 3 survivorsdefibrillation asystole. No survivors in primary asystole Zoll (1956; 23)In-hospital25/34 patients with Stokes-AdamsMechanical capture with long-Prompt use of device after rhythm attacksterm survivors in the 25 withnoted ventricular standstill 249

Pacing Techniques H

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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 incre- mental 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 elec- trode meant that the current density was very high at the electrode–skin 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 T

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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 V

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 patient’s spontaneous rate.

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 circum- stance. 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 intra- cavitary 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 con- tact 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 postdefibril- lation. Hedges defined an early period of 5 minutes or less of asystolic CA as an impor- tant 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 cap- turing 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.

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