Defibrillation has been defined as “the arrest of fibrillation of the cardiac muscle (atrial or ventricular) with restoration of the normal rhythm if successful.”¹ For practical purposes defibrillation is a definitive way in which the rescuer uses electricity in an attempt to convert a patient’s lethal rhythm into a viable one. Although exact statistics are not available, the AHA estimates that with early defibrillation (within 5 to 7 minutes) only 30% to 45% of cardiac arrest patients will survive the event, but without it 95% will die before reaching the hospital. ²

In addition to being able to recognize dysrhythmias, the emergency nurse must be knowledgeable of current evidence-based interventions for each abnormal rhythm. The first step is to be familiar with the equipment used at your facility. Is the defibrillator monophasic or biphasic? Does it function as hands-off only or paddles only? Can it pace, defibrillate, and synchronize cardiovert, or is it only an automated external defibrillator (AED)? Before using the defibrillator it is important to be sure that the machine either is plugged in or has a fully charged battery. This maintenance procedure should be performed daily to ensure that the defibrillator will be fully functional in the event of an emergency.

Previously the standard monophasic defibrillators allowed electrical current to flow in only one direction. With the advancement of technology, biphasic defibrillators have evolved, which allow the energy to flow in both directions. With biphasic energy delivery the amount of energy required to convert a lethal rhythm is significantly reduced. When deciding on the energy needed for defibrillation or synchronized cardioversion, confirm if the defibrillator is monophasic or biphasic and be aware of the manufacturer’s recommendations for energy delivery.

After confirming that the patient’s rhythm requires defibrillation, place the adhesive electrode pads (if the hands-off device is being used) on the patient’s bare chest. One pad goes to the upper chest just right of the sternum and the other at the apex of the heart on the patient’s left lateral chest, under the left breast. If paddles are used, they are held firmly in the same locations after being covered with conduction gel or placed on commercially prepared defibrillator pads (Figure 31-6).

Anterior/posterior placement may also be used with the hands-free method and is indicated when repeated or long-term placement may be necessary. If the patient has any implanted devices, pad/paddle placement may need to be slightly altered. Do not place the pad/paddle directly over the implanted device, and external devices should be at least 1 inch away. To deliver the defibrillation the machine must be turned on and the desired mode selected. It is important to be sure that the “defib” mode is engaged. Next the energy level must be selected/programmed in and the machine charged. When fully charged the machine will sound an alert. It is at this time that the rescuer will loudly announce that a shock is going to be delivered, “I’m clear, everybody clear,” and physically look to verify that all personnel are free from contact with the patient. To deliver the energy via the pads, press and hold the appropriate button on the device until the shock is delivered; with the paddles, press the discharge buttons on the paddle handles simultaneously. In the defibrillation mode the shock will be delivered immediately; rescuers should resume chest compressions immediately after the shock is delivered.

Another electrical delivery device available is the AED. There are many versions of this self-contained defibrillator available, and it is an integral part of the public access defibrillation program. Some health care facilities have chosen to place these lifesaving devices throughout their buildings and on low-acuity units where need is infrequent and staff are not trained in advanced resuscitation skills. The vast majority of AEDs use biphasic technology; some are fully automated with no oscilloscope, whereas others are semiautomated and require the user to have rhythm-recognition skills. Both types of AED use only “hands-free” defibrillation. Once properly placed on the patient, the device will analyze the rhythm and decide if a shock is needed. The fully automated AED will deliver the shock automatically, whereas the semiautomated AED requires the rescuer to follow the audible instructions step-by-step to deliver the shock. Introduction and training for AEDs are done in basic life support classes. In an effort to assist people with remembering the steps, the PAAS mnemonic was developed: power, attach, analyze, shock. As with all electrical devices, use the safety concepts discussed earlier.

Successful defibrillation depends on multiple factors. The reason the patient arrested is important. Determining the cause will be instrumental in correcting the issue and preventing reoccurrence. Using the AHA advanced cardiac life support (ACLS) guidelines, health care providers should consider reasons for the initial arrest (Table 31-4) and perhaps identify the reason for an unsuccessful defibrillation.

Synchronized cardioversion is used when either the patient has become hemodynamically unstable or pharmacologic interventions have been unsuccessful in managing sustained ventricular tachycardia, supraventricular tachycardia, atrial fibrillation, or atrial flutter. In synchronized cardioversion, energy is timed with the QRS complex and avoids shock delivery during the relative refractory period, which could produce ventricular fibrillation. Synchronized cardioversion decreases potential energy delivery during the vulnerable period of repolarization, that is, the T wave of the electrocardiogram (ECG) (Figure 31-7).

The procedure for cardioversion is the same as for defibrillation with three important distinctions: (1) the machine must be set on synchronous mode; (2) sedation should be given for the conscious patient if time allows; and (3) when the delivery button is pushed, there will be a slight delay in firing because the machine is sensing the R wave in order to deliver the energy at the precise moment. Anxiolytics such as diazepam (Valium) or midazolam (Versed) should be administered intravenously (IV) in small, incremental doses before energy delivery. The procedure should be explained to the patient and informed consent obtained whenever possible.

As has been previously discussed, it is important to determine the cause of the patient’s current condition. Potential treatable causes of cardiac arrest are found in Table 31-4. When possible a baseline 12-lead ECG should be obtained before and after the attempted cardioversion. Immediately after the procedure the patient’s cardiac rhythm, vital signs, and level of consciousness should be assessed and closely monitored until the patient is hemodynamically stable and returns to an acceptable rhythm. Complications of cardioversion include asystole, junctional rhythms, premature ventricular contractions (PVCs), ventricular tachycardia, ventricular fibrillation, embolization, and return to the original dysrhythmia.

Another method to convert a patient’s rhythm is through manual stimulation of the vagus nerve using a Valsalva maneuver such as causing the patient to gag or vomit. Stimulation of the vagus nerve will slow the heart rate and may terminate the dysrhythmia. In the past, ocular pressure and application of ice water to the patient’s face have been used; however, these methods are no longer recommended.

The physician may try carotid sinus massage to convert the rhythm. This is accomplished by placing pressure on the carotid bodies, which stimulates the baroreceptors and therefore the parasympathetic branch of the autonomic nervous system. This stimulation decreases blood pressure and heart rate. Only one side should be done at a time. Before attempting this procedure the physician should auscultate the carotid arteries for bruits. Bruits are produced by turbulent flow through the carotid arteries and are suggestive of atherosclerotic plaque in the artery. If any of this plaque were dislodged during the procedure, the patient would be at risk for a stroke. If a bruit is heard, carotid massage is contraindicated. If no bruits are heard and the procedure will be attempted, the patient should be supine on supplemental oxygen and have at least one patent IV access. Before, during, and after the attempt the patient should be closely monitored. In more than 75% of the population, preferential massage of the right carotid body affects the SA node, whereas left carotid body massage affects the AV node. Even when the SA node is completely shut down, the AV node can provide pacemaker activity. If the left side is massaged first, complete block of the AV node could occur and lead to a slow ventricular rate. Pressure must be applied gently to the carotid artery just below the mandible and in small, circular motions, rotating the fingers backward and medially. Carotid massage should not exceed 5 to 10 seconds and should be discontinued sooner if the rhythm changes. Even when properly performed, carotid massage may cause asystole for 15 to 30 seconds, followed by a few idioventricular complexes before a new pacemaker site becomes active. Emergency resuscitation equipment and medications should be readily available whenever carotid massage is performed. If carotid massage is successful, continue to monitor the patient for several hours. Complications of carotid massage include further dysrhythmias (e.g., ventricular tachycardia, ventricular fibrillation, asystole), stroke, cerebral anoxia, and seizures. ¹

A pacemaker is an electrical device that may restore an adequate heart rate and cardiac output. It can be used either via the transvenous or transcutaneous routes. A transcutaneous pacemaker (TCP) is a temporary intervention for patients experiencing symptomatic, unstable bradycardia, and second- or third-degree heart blocks because it is easily applied and managed until the patient can receive definitive treatment. The TCP can be applied by following these steps: (1) place the pacing electrodes on the patient’s bare chest as recommended by the manufacturer; (2) turn the pacemaker on, and set the demand rate as ordered by the physician (usually between 60 and 70 beats/min); and (3) turn up the milliamperes (mA) current slowly, increasing the dose until capture occurs with pacer spikes noted on the patient’s monitored rhythm. Keep the pacer’s mA at the lowest level possible that still maintains electrical capture (pacer spikes) and mechanical capture (patient’s pulse) and at a rate that keeps the patient clinically stable. Continuous pacing can be uncomfortable; therefore analgesia or anxiolytics should be considered.

Patients with complete heart block may be unable to electrically or mechanically respond to the pacemaker stimulus. Successful pacing depends on the condition of the myocardium. Mechanical capture is evaluated by the presence of a pulse consistent with paced beats. Both types of capture (electrical and mechanical) must be present for pacing to be considered effective. Two major reasons for lack of capture are acidosis and hypoxemia. Evaluate the patient’s oxygen saturation and acid-base levels to determine if further airway or ventilatory interventions are needed. If there is a lack of pacer spikes, begin by checking the TCP electrodes followed by inspecting all the wires and connections. If necessary replace electrodes to ensure contact between external pacing electrodes and skin surface is adequate. Skin should be clean and dry before electrode application. Tincture of benzoin may be used to improve adherence to the skin if the patient has been diaphoretic.

The implantable cardioverter-defibrillator (ICD) is a small generator that is used in patients at risk for life-threatening dysrhythmias—especially ventricular dysrhythmias. The ICD device is surgically placed under the skin in the chest wall just below the clavicle or in the abdominal cavity. This minigenerator monitors the patient’s rhythm, providing pacing, cardioversion, or defibrillation based on the patient’s needs, device capability, and programming.

When a patient with an ICD requires external defibrillation because the implanted device has malfunctioned or failed, it is important to know how to perform this intervention in a safe and effective manner. Defibrillator paddles or hands-free adhesive patches must not be placed directly over the ICD device. If standard paddle/patch placement and defibrillation attempts are unsuccessful, the resuscitation team should try the anterior-posterior placement for defibrillation. Health care professionals who have direct physical contact with the patient may experience a slight harmless tingling sensation when the ICD device fires. If the ICD fires inappropriately, the device can be deactivated by placing a magnet over the ICD generator. ¹

The use of IV fluids during resuscitation must be determined on an individual patient basis. Some patients may need crystalloid fluid boluses secondary to volume loss, whereas others may be in a fluid overload state and need to have intake strictly limited. In addition to the patient’s current status, it is important to gather as much of the health history as possible because this information will influence the amount, rate, and type of IV fluids administered. After every intervention it is necessary to reassess and evaluate the patient’s response. Because of adverse effects on cerebral tissue, dextrose-containing solutions are not recommended during resuscitation; instead the fluids of choice are normal saline or lactated Ringer’s solution.

Emergency drug therapy depends on the patient’s cardiac rhythm, 12-lead ECG, and hemodynamic status. Table 31-5 provides an overview of commonly used emergency medications. The first-line drug in management of cardiac arrest, specifically asystole, pulseless electrical activity (PEA), VF, and pulseless VT is either epinephrine or vasopressin. ¹ It is important to remember that the management of VF and pulseless VT requires immediate defibrillation followed by chest compressions before the administration of medications.

Patients with ventricular dysrhythmias associated with cardiopulmonary arrest may benefit from amiodarone (Cordarone) administration. Other antidysrhythmic agents considered for management of patients with VF or pulseless VT include lidocaine (Xylocaine), magnesium, and procainamide (Pronestyl). After the ventricular dysrhythmia is controlled, an infusion of the converting agent is necessary to maintain therapeutic drug levels. Antidysrhythmics should not be given to patients with third-degree AV block, with an escape rhythm, or with bradycardia and PVCs. Ectopic beats may contribute to the patient’s cardiac output; therefore lidocaine could effectively reduce output and cause further decompensation or asystole.

Bradycardic dysrhythmias are initially managed with atropine, which blocks stimulation of the vagus nerve. Atropine may also be used for asystole and PEA. Atropine may not be effective for high-degree AV block dysrhythmias. Isoproterenol (Isuprel) is a β-adrenergic agonist and may be used to increase cardiac output in bradydysrhythmias. Routine use of isoproterenol is not recommended because of effects on ventricular irritability; however, it is considered a first-line drug for the heart transplant patient with symptomatic bradycardia. Atropine is not used for heart transplant patients because the vagus nerve is not reattached during the transplant. Bradycardic rhythms that affect hemodynamic stability may ultimately require cardiac pacing.

Supraventricular rhythms impair effective cardiac output by decreasing cardiac filling time and may decrease the patient’s hemodynamic stability. Adenosine (Adenocard) is used to treat reentry dysrhythmias. It is an extremely fast-acting drug with a half-life of less than 10 seconds. For this reason it must be given rapidly and in a proximal vein, then followed with a 20-mL saline bolus. Side effects include flushing, dyspnea, hypotension, chest pain, transient bradycardia, transient asystole, and ventricular ectopy. These side effects will usually terminate spontaneously without further medical or nursing interventions. Other pharmacologic agents such as ibutilide, β-adrenergic blocking drugs (e.g., metoprolol [Lopressor]), and calcium channel blocking agents (e.g., verapamil [Calan] and diltiazem [Cardizem]) can be used for controlling ventricular response rate in patients with supraventricular tachycardias (e.g., atrial fibrillation, atrial flutter, supraventricular tachycardia, atrial tachycardia). Monitor for bradycardia and hypotension when administering these medications.

Other miscellaneous drugs that may be used during cardiac arrest include sodium bicarbonate, calcium, and magnesium sulfate. Sodium bicarbonate is reserved for specific clinical situations including hyperkalemia, preexisting bicarbonate-responsive acidosis, and tricyclic antidepressant overdose. Magnesium is considered useful in the treatment of torsades de pointes, suspected hypomagnesaemia, and refractory ventricular fibrillation. Calcium, an ion essential for myocardial contractions and impulse formation, is recommended for hyperkalemia, hypocalcemia, and calcium channel blocker toxicity.

During cardiopulmonary arrest, hemodynamic status is unstable and requires intervention to stabilize not only the patient’s cardiac rhythm but also the cardiovascular system. Table 31-6 reviews vasoactive drugs more commonly used during cardiopulmonary emergencies. ^{1.9. and 22.} Refer to Table 31-7 for an overview of cardiovascular drugs that can be given via the endotracheal tube or intraosseous route when IV access cannot be established. ^{1.9. and 22.}