Page 670 - Cardiac Nursing

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646 PA R T I V / Pathophysiology and Management of Heart Disease
DISPLAY 27-5 Arrest and Alive—Scientific Evidence for Use of Amiodarone
ARREST Trial—Amiodarone in Out-of-Hospital Resuscita- ALIVE Trial—Amiodarone versus Lidocaine in Prehospital
tion of REfractory Sustained Ventricular Tachyarrhyth- Ventricular Fibrillation Evaluation
mias Methods: Patients were enrolled if they had an out-of-hospi-
Methods: Patients were enrolled if they had three or more tal VF arrest resistant to total of four shocks and one
unsuccessful shocks for VF or pulseless VT in an out-of- dose of epinephrine; or if they had a recurrence of VF af-
hospital cardiac arrest. In a randomized, double-blind, ter initial success. Patients were randomized in a double-
placebo controlled study patients were either randomly blind manner to receive either IV amiodarone plus
assigned to receive 300 mg of IV amiodarone (246 lidocaine placebo (179 patients) or IV lidocaine plus
patients) or placebo (258 patients). amiodarone placebo (165 patients). The primary
Results: Patients in the amiodarone group were more likely endpoint was survival to hospital admission.
to survive to be admitted to the hospital. Forty-four per- Results: Those patients receiving amiodarone had a higher
cent of patients in the amiodarone group survived to hos- rate of survival to hospital admission than those receiv-
pital admission compared to 34% in the placebo group. ing lidocaine (22.8% in amiodarone group versus 12.0% in
There was no statistical difference in survival to hospital lidocaine group). However only 5% of amiodarone group
discharge between the two groups. survived to hospital discharge, and 3% of lidocaine group
Conclusion: Patients in refractory VT/VF treated with amio- survived to hospital discharge.
darone in out-of-hospital cardiac arrests have a higher Conclusion: Amiodarone shows clinical effectiveness in
rate of survival to hospital admission. Further investi- the early stages of resuscitation. There appears to be no
gation is warranted to see if the benefits extend to hospi- indication for the administration of lidocaine in the out-
tal discharge. (From Kudenchuk, P. J., Cobb, L. A., Copass, of-hospital setting for shock-resistant ventricular fibrilla-
M. K., et al. [1999]. Amiodarone for resuscitation after tion. (From Dorian, P., Cass, D., Schwartz, B., et al. [2002].
out-of-hospital cardiac arrest due to ventricular Amiodarone as compared with lidocaine for shock-
fibrillation. New England Journal of Medicine, 341, resistant ventricular fibrillation. New England Journal
871–878.) of Medicine, 346, 884–890.)
shown to be effective in terminating polymorphic VT associated tion idioventricular rhythms, and bradysystolic rhythms. Like asys-
with long QT (torsades de pointes) (class IIa for torsades). Magne- tole, the prognosis of patients with PEA is very poor unless the un-
sium has not been shown to be effective with polymorphic VT and derlying cause can be identified and treated appropriately. There-
32
normal QT interval. Antiarrhythmic drugs are delivered by a bo- fore, the highest priority is to find the correctable cause while
lus during cardiac arrest; however, after a return of spontaneous cir- maintaining the patient’s airway, breathing, and circulation. Com-
culation (ROSC), they are often converted to infusions. mon correctable causes of electromechanical dissociation include
hypovolemia, cardiac tamponade, tension pneumothorax, hypox-
Asystole emia, and acidosis. Massive damage from MI, prolonged ischemia
The prognosis for patients in asystole is extremely poor. Asystole during resuscitation, and pulmonary embolism are less correctable
usually is the result of end-stage heart disease or prolonged cardiac causes. Patients in profound shock of any cause initially may pres-
arrest. The focus for treating asystole is effective CPR with mini- ent with PEA. Hypovolemia is assessed by history and lack of neck
mal interruptions, providing ventilation with an advanced airway, vein distension; it is treated by volume replacement. Tension pneu-
and treating reversible causes. When asystole is first recognized a mothorax is assessed by history and neck vein distension; it is
second lead configuration should be checked to reconfirm asys- treated by needle aspiration, chest tube insertion, or both. Cardiac
tole. The defibrillator should also be checked quickly to assure tamponade is assessed by history and neck vein distension; it is
that no leads have been disconnected from the patient or defibril- treated by pericardiocentesis or thoracotomy. Hypoxemia is as-
lator/monitor. Vasopressors (epinephrine or vasopressin), and at- sessed by history and arterial blood gases and is treated by improv-
ropine are the treatment options in cardiac arrest with asystole and ing oxygenation and ventilation. Acidosis is also assessed by history
are used in an attempt to induce spontaneous electrical activity. and arterial blood gases, and is treated by improving CPR tech-
Asystole should not be defibrillated. There have been no studies nique and hyperventilating the patient. If bradycardia is present,
that have documented an improvement in survival by shocking then atropine may be administered in an attempt to increase heart
asystole. Also, there have been no trials to show benefit from tran- rate. ACLS presents the most common cause of PEA as “H’s” (hy-
scutaneous pacing for asystole. Asystole and PEA are both pulse- povolemia, hypoxia, hydrogen ion, hypo-/hyperkalemia, hypo-
less and nonshockable conditions. The right side of the pulseless glycemia, hyperthermia) and “T’s” (toxins, tamponade, tension
arrest algorithm should be utilized to review all the steps to take pneumothorax, thrombosis, trauma) and can be viewed at the bot-
in treating asystole (Fig. 27-3). CPR and resuscitation efforts tom of the pulseless arrest algorithm (Fig. 27-3). 32,33
should be ceased if it is determined that the patient has a valid do
not attempt resuscitation order, has signs of irreversible death, or Management of Impending
no physiologic benefit can be expected. 32,33
Cardiac Arrest
Pulseless Electrical Activity Ventricular and Supraventricular
PEA is an organized rhythm without a pulse, and includes electro- Tachycardia
mechanical dissociation, pseudo-electromechanical dissociation, The tachycardia algorithm (Fig. 27-4) directs rescuers to focus on
idioventricular rhythms, ventricular escape rhythms, postdefibrilla- the patient and determine the hemodynamic stability of the