175

showed significantly lower rates of 1-month survival and 1-month survival with

favorable neurologic outcomes in out-of-hospital cardiac arrest patients with

shockable rhythm, who received epinephrine before hospital arrival, relative to

patients who did not receive epinephrine (p < 0.001).

On the basis of these trials, it would be reasonable to use a single dose of

vasopressin 40 units as an alternative to either the first or second dose of epinephrine

1 mg in the treatment of VF (or pulseless VT).

CASE 15-9, QUESTION 3: One of the physicians delivering ACLS for M.N. wants to initiate corticosteroid

therapy. What is the evidence supporting the use of corticosteroid therapy in patients experiencing cardiac

arrest?

A randomized, double-blind, placebo-controlled, parallel-group trial performed

by Mentzelopoulos et al.

176 assessed the impact of using two different strategies for

managing in-hospital cardiac arrest patients on: (a) survival to hospital discharge

with favorable neurologic status; and (b) probability for return of spontaneous

circulation for 20 minutes or longer. One group of patients received epinephrine (1

mg/CPR cycle), vasopressin (20 IU/CPR cycle), and corticosteroid therapy

(methylprednisolone 40 mg during first CPR cycle, then hydrocortisone 300 mg/day

[for post-resuscitation shock] for up to 7 days, followed by taper). The control group

received epinephrine in combination with saline placebo. Epinephrine–vasopressin–

corticosteroid recipients exhibited superior rates of probability for return of

spontaneous circulation for ≥20 minutes (83.9% vs. 65.9%; OR, 2.98; 95% CI, 1.39–

6.40; p = 0.005), and survival to hospital discharge with favorable neurologic status

(13.9% vs. 5.1%; OR, 3.28; 95% CI, 1.17–9.20; p = 0.02), compared to the control

group.

CASE 15-9, QUESTION 4: Because M.N. has an IV site and the time from cardiac arrest to ACLS was

brief, epinephrine was chosen and a 1-mg bolus was given, followed with a 20-mL normal saline flush. The arm

was elevated for 20 seconds to ensure adequate delivery. Thirty seconds after administration a 200-J shock is

given (via biphasic manual defibrillator), but it fails to convert VF. What can be done now?

The most recently updated ACLS guideline calls for the use of amiodarone in

cases of VF or pulseless VT that do not respond to CPR, shocks, and a

vasopressor.

167

IV AMIODARONE AND LIDOCAINE

The effect of amiodarone on VF or pulseless VT was studied in the ARREST

(Amiodarone for Resuscitation of Refractory Sustained Ventricular

Tachyarrhythmias) trial.

171 This study was conducted in patients who experienced

cardiac arrest in an out-of-hospital situation with therapy given by paramedics in the

field. Patients who failed three stacked shocks and one dose of epinephrine with an

electrical countershock were randomly assigned to amiodarone 300 mg IV bolus or

placebo. This was followed by other antiarrhythmic agents historically used in ACLS

(2,000 guidelines: lidocaine, procainamide, or bretylium) if the clinicians desired.

Amiodarone significantly increased the chance of survival to hospital admission

(44% vs. 34% of placebo group; p = 0.03), but survival to hospital discharge was

not changed. Of note, 66% of patients received antiarrhythmic drug treatment for

pulseless VT or VF after amiodarone administration.

The ALIVE (Amiodarone vs. Lidocaine in Ventricular Ectopy, n = 347) trial

directly compared IV amiodarone 300 mg to lidocaine 1 to 1.5 mg/kg bolus.

173

In this

trial, patients needed to fail three stacked shocks and epinephrine plus an additional

shock to be eligible for randomization to either amiodarone or lidocaine.

Amiodarone was given as an initial dose of 5 mg/kg followed by a shock. If

unsuccessful, a dose of 2.5 mg/kg was given followed by a subsequent shock.

Lidocaine was given as a 1.5 mg/kg bolus followed by a shock. If therapy failed, then

a second bolus of 1.5 mg/kg was used with a subsequent shock. If the first

antiarrhythmic drug failed, other routine antiarrhythmic drugs for cardiac arrest (per

2000 ACLS guidelines: e.g., procainamide, bretylium) could be tried. Patients given

amiodarone were 90% more likely to experience the primary outcome, survival to

hospital admission, than those given lidocaine (p = 0.009). Unfortunately, no

significant advantage to hospital discharge occurred (5% vs. 3%).

On the basis of these findings, amiodarone is the only antiarrhythmic agent with

proven ability to improve return of spontaneous circulation and short-term survival

versus other antiarrhythmic therapy. However, it has not yet been shown to improve

survival to hospital discharge.

M.N. is at serious risk of death as a result of VF. However, as long as M.N.

remains in VF, it is appropriate to continue active therapy. If M.N. degenerates into

asystole after this long period of VF, then the resuscitation efforts should be

discontinued. However, if a patient only had a brief period of VF before having

asystole, it is prudent to apply active therapy.

Pulseless Electrical Activity

CASE 15-10

QUESTION 1: J.D. is an 80-year-old woman who experiences cardiac arrest in the hospital. J.D. was in

respiratory failure upon admission to the ED, where she underwent immediate intubation, had a peripheral IV

placed, and upon transfer to the MICU, placed on assist/control mechanical ventilation with FiO2

of 100%. A

rhythm is noted on the monitor, but no femoral pulse is felt. M.N. is in PEA. How should J.D. be treated?

The clinical situation in which there is organized electrical activity on the monitor

without a palpable pulse is called PEA. Although electrical activity is present, it

fails to stimulate the contractile process. Virtually all patients in true PEA die.

However, not all patients who present with a rhythm and no pulse are in true PEA.

Therefore, it is important to rule out treatable causes in patients who appear to be in

PEA. The major treatable causes are hypovolemia, hypoxia, acidosis, hyperkalemia,

hypokalemia, hypothermia, cardiac tamponade, pulmonary embolism, acute coronary

syndrome, trauma, and drug overdose. In the absence of an identifiable cause, the

focus of resuscitation is to administer high-quality CPR, and after the initial rhythm

check, resume CPR during the establishment of IV or IO (intraosseous) access.

167

p. 331

p. 332

Figure 15-15 Asystole. There is no electrical activity detected in the heart resulting in a very low amplitude

undulating waveform.

Once IV or IO access becomes available, administer epinephrine 1 mg every 3 to

5 minutes or give one dose of vasopressin 40 units in place of the first or second

dose of epinephrine, as published studies have failed to demonstrate a survival

advantage of either vasopressor for patients experiencing PEA.

167,169,170

Asystole

CASE 15-11

QUESTION 1: K.K., a 73-year-old man, has a past medical history significant for hypertension and

diverticulitis. Upon arrival at the OR for surgical correction of pericardial and pleural effusions, K.K. received

etomidate, fentanyl, lidocaine, and succinylcholine. During placement of a double-lumen endotracheal tube, K.K.

goes into cardiac arrest. The ECG shows a flat line, and the patient is determined to be in asystole (Fig. 15-15).

Is this rhythm treatable?

Lack of electrical activity or asystole, like PEA, carries a grave prognosis. Its

development usually indicates a prolonged arrest, which may explain its poor

response to treatment. However, a few patients will go directly from a sinus rhythm

into asystole and may be resuscitated. Enhanced parasympathetic tone, possibly

attributable to a vagal reaction, manipulation of the airway from intubation,

suctioning or insertion of an oral airway, or chest compression, may play a role in

inhibiting supraventricular and ventricular pacemakers.

168

A post hoc analysis performed by Wenzel et al.

168 demonstrated superior survival

rates at the time of hospital admission in vasopressin-treated patients, compared with

epinephrine-treated patients. However, no difference in intact neurologic survival

was noted between the two treatment groups. Consequently, providers may choose to

administer vasopressin 40 units IV (in place of the first or second dose of

epinephrine) or epinephrine 1 mg IV every 3 to 5 minutes.

CASE 15-11, QUESTION 2: Does the timing of epinephrine dosing impact survival to hospital discharge in

patients with non-shockable rhythms (asystole or PEA)?

A post hoc analysis of data from the Get With the Guidelines-Resuscitation study

showed a stepwise reduction in survival to hospital discharge (primary study end

point) with each 3-minute delay to epinephrine: (a) 1 to 3 minutes (OR 1.0, reference

group); (b) 4 to 6 minutes (OR, 0.91; 95% CI, 0.82–1.00; p = 0.055); (c) 7 to 9

minutes (OR, 0.74; 95% CI, 0.63–0.88; p < 0.001); and (d) >9 minutes (OR, 0.63;

95% CI, 0.52–0.76; p < 0.001).

177

CASE 15-11, QUESTION 3: What is the long-term prognosis for patients with non-shockable rhythms?

Goto et al.

175 assessed the impact of pre-hospital epinephrine administration on

long-term outcomes seen in out-of-hospital cardiac arrest patients with nonshockable rhythms.

176 Epinephrine recipients showed superior 1-month survival rates

compared to patients who did not receive pre-hospital epinephrine (3.9% vs. 2.2%;

p < 0.001). However, pre-hospital administration of epinephrine did not result in

improved 1-month favorable neurologic outcomes (p = 0.62).

KEY REFERENCES AND WEBSITES

A full list of references for this chapter can be found at

http://thepoint.lww.com/AT11e. Below are the key references and websites for this

chapter, with the corresponding reference number in this chapter found in parentheses

after the reference.

Key References

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Giugliano RP et al. Edoxaban versus warfarin in patients with atrial fibrillation. N EnglJ Med. 2013;369:2093. (84)

Granger CB et al. Apixaban versus warfarin in patients with atrial fibrillation. N EnglJ Med. 2011;365:981. (83)

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Circulation. 2014;130:e199–e267 (11).

Le Heuzey et al. A short-term, randomized, double-blind, parallel-group study to evaluate the efficacy and safety of

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Electrophysiol. 2010;21:597. (75)

Mentzelopoulos SD et al. Vasopressin, steroids, and epinephrine and neurologically favorable survival after inhospital cardiac arrest: a randomized clinical trial. JAMA. 2013;310:270. (176)

Morillo CA et al. Radiofrequency ablation vs. antiarrhythmic drugs as first line treatment of paroxysmal atrial

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Pederson CT et al. HER/HRS/APHRS expert consensus on ventricular arrhythmias. Heart Rhythm. 2014;11:e166.

(103)

Key Website

Blaufuss Medical Multimedia Laboratories ECG Tutorial. http://www.blaufuss.org.

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