When ventricular fibrillation occurs in a ICU the first person reaching the client should?

KEY POINTS

1. Biphasic waveform cardioversion is safe and equally effective as monophasic cardioversion, using much lower energy with reduced post-shock complications such as cardiac dysfunction, dysrhythmias, and skin burns.

2. Defibrillation or unsynchronized cardioversion is indicated in any patient with pulseless VT/VF or unstable polymorphic VT, where synchronized cardioversion is not possible.

3. Synchronized cardioversion is utilized for the treatment of persistent unstable tachyarrhythmia in patients without loss of pulse. Amongst this category, AF remains the most frequently encountered.

4. In critically ill patients, unstable supraventricular tachyarrhythmias benefit from individualized therapy such as inotrope and vasopressor support, antiarrhythmic medications or mechanical ventilation and not necessarily electrical cardioversion as the first treatment.

5. It is important to become familiar with the cardioversion device available, the appropriate energy settings and the correct placement of the paddles to ensure effective and timely shock administration.

The incidence of cardiac arrhythmias in critically ill patients has been shown to be considerable, ranging from less than 50% in trauma patients to more than 90% in those admitted with a primary cardiac illness.1 In the ICU, the most common arrhythmias are atrial fibrillation (AF) and ventricular tachycardia (VT).2 These arrhythmias vary in their presentation from incidental findings on telemetry to symptomatic episodes with profound compromise in cardiac and pulmonary function. Rapid diagnosis and critical interventions are important as these arrhythmias cause hemodynamic instability, prolong ICU length of stay, and increase morbidity and mortality.2,3

Electrical current or shocks delivered to the chest to terminate ventricular fibrillation (VF) was first reported in the 1950s.4 Today, defibrillation is an established component of the Advanced Cardiovascular Life Support (ACLS) algorithm for pulseless VT/VF. The delivery of an electrical shock results in simultaneous depolarization of the myocardium making the heart refractory to the ongoing disordered electrical activity. This allows for the interruption of the underlying malignant rhythm and reestablishment of the normal electrical rhythm of the heart.5,6

In the case of tachyarrhythmias where the rhythm is organized and the patients have a palpable pulse, an electrical shock is given as a synchronized cardioversion. Cardioversion refers to the delivery of an electrical shock that is timed to the peak of the R wave on the EKG. This synchronization ensures that the electrical stimulation occurs only during the refractory period of the cardiac cycle minimizing the risk of iatrogenic arrhythmias. The literature on cardioversion can be confusing as many alternate terms such as external cardioversion, synchronized cardioversion, DC cardioversion, and transthoracic DC cardioversion are used interchangeably.

Traditionally monophasic waveform cardioverters were used until the introduction of biphasic waveform cardioversion in the mid-1990s. Increasingly more cardioverters in the ICU are biphasic. Biphasic waveform cardioversion is safe and as equally effective as monophasic cardioversion, using much lower energy with reduced post-shock complications such as cardiac dysfunction, dysrhythmias, and skin burns.7,8,9 It is important for the intensivist to be aware of the type and model of cardioverter/defibrillator available in the units they cover so as to ensure appropriate delivery of electrical shocks.

Synchronized cardioversion is utilized for the treatment of persistent unstable tachyarrhythmia in patients without loss of pulse. Amongst this category, AF remains the most frequently encountered. Other unstable tachyarrhythmias with intact pulses where cardioversion has been demonstrated to be effective include atrial flutter, atrial ventricular nodal reentrant tachycardia (AVNRT), atrial ventricular reentrant tachycardia (AVRT) with pre-excitation pathways and monomorphic regular ventricular tachycardia.

Defibrillation or unsynchronized cardioversion is indicated in any patient with pulseless VT/VF or unstable polymorphic VT where synchronized cardioversion is not possible. These are fatal arrhythmias that require prompt recognition and early correction by administration of electrical shock. In these circumstances, defibrillation therapy would take precedence over all other treatments being provided to the ICU patient except when providing the initial cycles of CPR prior to shock delivery per ACLS protocol or establishing an adequate airway when hypoxemia due to an inadequate airway is causing the arrhythmia.

The parameters for defining an unstable arrhythmia as mentioned in the advanced cardiovascular life support guidelines includes any arrhythmia that is causing hypotension, altered mental status, signs of shock, ischemic chest discomfort or acute heart failure. However, ICU patients are frequently admitted with similar symptoms as part of their primary critical illness. In such situations, unstable supraventricular tachyarrhythmias benefit from individualized therapy such as inotrope and vasopressor support, antiarrhythmic medications or mechanical ventilation and not necessarily electrical cardioversion as the first treatment. It is imperative that the intensivist is able to quickly discern if the arrhythmia is the primary cause of a patient’s instability, and where it is merely a marker of the patient’s illness.

Tachyarrhythmias seen in the ICU setting are often a product of the complex interplay between the patient’s severe illness and the interventions being performed. The presence of multi-organ failure, concomitant sympathetic and neurohumoral surges, arrhythmogenic drugs and invasive surgical therapies modulate the pathways for arrhythmia generation as well as their response to conventional therapies. The use of vasopressors and inotropes present a challenge to the control of tachyarrhythmias that requires titrating the dose and duration of these therapies, avoiding more arrhythmogenic agents such as dobutamine or dopamine. Recognizing the need for prompt source control in septic patients, controlling electrolyte disturbances in diabetic ketoacidosis, minimizing autonomic fluctuation following a subarachnoid bleed, and closely monitoring and managing pain, anxiety, agitation, oxygenation, and delirium are some examples of addressing the primary illness which can aid in stabilizing cardiac issues.

Cardioversion is still warranted in situations where the patient’s hemodynamic status remains compromised despite the above interventions. While successful, post cardioversion tachyarrhythmias tend to recur in patients with sepsis and multiorgan failure. Furthermore the delivery of successive electrical shocks in these patients may be very poorly tolerated as compared to other patient populations. It is thus for the intensivist to make judicious utilization of cardioversion therapy understanding all the benefits and risks involved.

New onset AF occurs in about 46% of patients with septic shock and is associated with prolonged ICU stay and a trend towards increased mortality.3 It is believed that the increased adrenergic activity during sepsis and septic shock contributes to the frequent occurrence of arrhythmias in the ICU, and in these patients, rate control and maintaining sinus rhythm can be challenging unless the underlying pathology has been addressed. Patients with AF of more than seven days duration, dilated atria on echocardiogram, or heart failure also have an increased risk of recurrence after cardioversion.10 The use of amiodarone infusion before and after electrical cardioversion increases the chances of maintaining sinus rhythm.

Narrow complex tachycardias include atrial flutter, atrioventricular nonreentrant tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT) and junctional tachycardia. These rhythms tend to occur in a paroxysmal manner often converting back and forth on their own. Hemodynamic instability or persistent and symptomatic SVT despite medical therapy (IV beta-blocker, calcium channel blocker, or adenosine administration) is an indication for urgent cardioversion.

Synchronized cardioversion can be performed in unstable patients with a regular monomorphic VT in the presence of a pulse. Patients with irregular or polymorphic VT should however be managed with defibrillation. It is important to note that synchronization of the electrical discharge with the QRS complex in monomorphic VT may be very challenging to achieve. Thus, patients who present with signs of clinical instability such as hypotension, chest pain, acute pulmonary edema, heart failure, and change in mental status, should receive urgent unsynchronized defibrillation if attempts at synchronization are unsuccessful.

VF and pulseless VT are managed by defibrillation and CPR until return of spontaneous circulation (ROSC) with a perfusing rhythm has been established as outlined in the advance cardiac life support (ACLS) protocol. Although improved survival has been linked to early defibrillation in VF, recent guidelines by the American Heart Association (AHA) emphasize the importance of immediate high quality chest compressions during cardiac arrest before attempting defibrillation even in the setting of VF or pulseless VT arrest.11 Care should be taken to observe for fine VF that can often appear on the cardiac monitor as asystole resulting in an overlooked opportunity for defibrillation.

See Table 92–1 for the initial energy requirements commonly used during cardioversion using monophasic and biphasic waveform cardioverters. In patients with AF causing hemodynamic compromise, start synchronized cardioversion at 120 Joules (J) using a biphasic defibrillator and increase up to 200 J during the subsequent shocks. Unstable atrial flutter or paroxysmal supraventricular tachycardia (PSVT) require much lower energy and cardioversion may be initiated at 50 J biphasic (100 J monophasic) initially, then 100 J if unsuccessful. If it fails to terminate the SVT, a higher follow-up shock of 200 J (360 J monophasic) may be delivered. Monomorphic VT with a pulse is treated with synchronized cardioversion with initial 100 J biphasic (100 J monophasic), and escalation of energy to 200 J biphasic (360 J monophasic) with each successive shock until sinus rhythm is achieved. Delivering an initial 120 J (200 J monophasic) defibrillation shock is usually sufficient to terminate VF or pulseless VT. If unsuccessful, energy can be escalated to 200 J (360 J monophasic) for subsequent shocks. In the case of polymorphic VT with pulse, defibrillation with similar energy settings (120 to 200J biphasic) are used as with pulseless VT.

Table 92–1Initial energy requirements commonly used during cardioversion.

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Table 92–1 Initial energy requirements commonly used during cardioversion.

Sedation and Analgesia

Delivering shocks can be painful, traumatic and may cause great anxiety in conscious patients receiving synchronized cardioversion or defibrillation. Short acting sedatives such as midazolam (0.02–0.03 mg/kg over 2–3 min) and or ketamine (1–2 mg/kg over 1–2 min), and analgesics such as fentanyl (0.5–1 mcg/kg) can be administered before the procedure. In patients who have a secured airway (eg, endotracheal intubation) and are more hemodynamically stable, propofol (eg, 0.3–1 mg/kg) is an effective short acting sedative that may be used in combination with an analgesic such as fentanyl. Only in the presence of experienced personnel (eg, anesthesiologist, intensivist), propofol can also be administered in smaller doses in nonintubated patients. In the elderly, administering lower doses of sedatives at less frequent intervals and at slower rates may be appropriate.

Application of Electrodes (Paddles or Pads)

The survival rate goes down 2.3% per minute until CPR is started and 1.1% per minute until a defibrillation shock is delivered.12 The early application of paddles or pads (electrodes) is a critical link in the management of arrhythmias with hemodynamic compromise. It allows for a shorter analysis time and quicker delivery of electric shocks.

The positioning of the electrodes on the thorax determines the transthoracic pathway and the flow of current delivered during cardioversion and defibrillation. Currently, there are two conventional positions accepted for electrode placement: the anterolateral and anteroposterior orientation [Figures 92–1(A) and 1(B)]. In the anterolateral position, a first electrode is placed on the right edge of the sternum along the second or third intercostal space (ICS), while the second electrode is placed laterally on the left at the level of fourth or fifth ICS along the mid-axillary line. In the anteroposterior position, the first paddle is placed as above and the second paddle is placed on the back between the tip of the scapula and the spine. The anteroposterior placement of the electrodes is preferred in patients with implantable cardioverter-defibrillator devices (ICDs) to avoid shunting of energy and damage to the implantable device. The electrodes should be maintained in contact with the skin using either conductive gel (with paddles) or by using self-adhesive pads instead. In the case of pads, care should be taken to ensure that they are well secured. This may be particularly difficult in the patient with excess hair or sweat. The electrode pads are then connected to the cardioverter through a wire with a plastic adaptor (usually colored) as indicated in Figure 92–2. Each cardioverter is provided with disposable electrode pads designed for that model.

Figure 92–1

Placement of the pads in an (A) anterolateral configuration and (B) anteroposterior configuration.

Figure 92–2

Attach cables to ensure tight connection between electrode pads and the cardioverter.

CPR Before Cardioversion

In cases such as in VF or pulseless VT, CPR should not be delayed and should be initiated immediately while preparing for defibrillation. The 2010 AHA Guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) recommends high quality CPR to be initiated for at least 90 to 180 seconds while the defibrillator pads and electrodes are being applied and before first defibrillation is attempted. It is believed that during VF, the myocardium is being depleted of oxygen and energy and that delivering CPR during this crucial period will provide the needed oxygen and energy, as well as increase the likelihood of terminating VF during defibrillation and rapid return of spontaneous circulation. Electrolyte imbalances such as hypocalcemia, hypokalemia and hypomagnesemia should also be corrected to improve successful cardioversion.

The following are basic steps for using the cardioverter:

1. Press the “ON” button to start operation of the defibrillator.

2. Most defibrillator brands are multifunctional and can be used as an automated external defibrillator (AED), manual defibrillator, external pacer or for ECG monitoring. Make sure that the device is set to defibrillator mode.

3. Apply the self-adhesive electrode pads to the patient’s bare chest using anterolateral or anteroposterior orientation [Figure 92-1(A) and 92-1(B)], then connect the electrode pads wire into the cardioverter via a plastic adaptor (usually color-coded, as in Figure 92–2).

4. Place the 3-wire ECG leads on the patient and connect them to the ECG slot of the defibrillator. Once connected, the monitor will display the ECG tracing and the heart rate.

5. Press the “ENERGY SELECT” button to set the initial or preferred energy for defibrillation (Figure 92–3).

6. For synchronized cardioversion, press the “SYNC” button and a marker above every QRS is displayed. The monitor also displays “Sync” once this function is turned on. The device automatically returns to asynchronous mode after each synchronized discharge. This means that the “Sync” button needs to be turned on if the first synchronized cardioversion is unsuccessful and a second synchronized shock is indicated. Note again that the defibrillator will not be able to deliver a shock for rhythms requiring unsynchronized cardioversion if the “Sync” button is turned on.

7. Once the preferred energy level is set, pressing the “CHARGE” button charges the defibrillator. A charge tone indicates that the charge is complete to the selected energy level (Figure 92–4).

8. Once the defibrillator is fully charged, a shock can be delivered by pressing the flashing “SHOCK” button. It is utmost important that the person in charge states “all clear” and checks that all personnel are clear of contact with patient, bed, or equipment before delivery of the shock. Occasionally, the defibrillator may not be able to deliver the required shock even after the “Shock” button is pressed. Check to make sure that the defibrillator is connected to a power supply or that battery power is sufficient as displayed by the battery indicator on the monitor, and that the “Sync” button is not inadvertently on in the setting of rhythms requiring unsynchronized cardioversion (Figure 92–5).

9. After the shock is delivered, the energy for each subsequent shock is automatically selected based on the energy level configured on the set-up. To escalate or change the energy level for the next shock, press the “ENERGY SELECT” button and return to step 5.

10. At anytime, an unwanted charge can be discharged by pressing the “DISARM” button.

Figure 92–3

Use the Energy Select button to choose the energy level delivered during the cardioversion.

Figure 92–4

Use the Charge button to charge the cardioverter.

Figure 92–5

Arrow- Synchronize Cardioversion On/Off Button.

There are a number of variables that influence the outcome of a cardioversion and/or defibrillation attempt. These can be grouped as patient characteristics such as body habitus, device characteristics including paddle size, waveform morphology and iatrogenic factors including administration of medications and ventilator support.

Electric shocks used in cardioversion and defibrillation are quantified by the amount of energy delivered. While this allows for the standardization of shocks delivered, it is important to understand that the determinant of an adequate shock is not the energy itself but the amount of electrical current that travels across the heart depolarizing the myocardium. The transmyocardial current generated is dependent directly on the energy level set and inversely related to the resistance/impedance offered by the circuit.

This resistance, termed as thoracic impedance, is determined by the electrode-to-skin interface, electrode pressure, body habitus and the phase of ventilation. Decreasing the interface between the skin and the paddle by placing more pressure on the paddles, applying adhesive or more conductive gel as well as delivering shocks during expiration decreases thoracic impedance and increases the effectiveness of cardioversion and defibrillation. Hairs should also be shaved off the chest if necessary to facilitate attachment of electrode pads to the skin.

Pad size is also an important determinant of transthoracic flow during delivery of shocks. A paddle or pad size with larger surface area has been associated with less thoracic resistance and less chances of myocardial injury.10 A standard adult electrode pad size usually measures about 8 to 12 cm and is commercially packaged and available for single use.

Observational studies have shown that persistent AF may be more easily converted using a hand-held paddle and the improved electrode-to-skin contact and reduced thoracic impedance are likely contributing to the higher success rate of cardioversion.11 However, there is no current data comparing the use of hand-held paddles and self-adhesive pad electrodes for other arrhythmias requiring cardioversion or defibrillation. Therefore, the decision to use which type of electrodes should base on equipment availability and the operator’s opinion regarding which electrodes are more likely to be effective in a particular patient.

There has been ongoing debate about the relative impact of the positioning of the electrodes on the outcome of the cardioversion attempt. An initial study from Germany demonstrated a statistically significant difference in the successful cardioversion of AF with anteroposterior positioning of the electrodes (96%) as compared to anterolateral position (78%).13 However subsequent studies have not demonstrated this benefit in a consistent manner.14 In the ICU it is often difficult to position patients for placement of posterior pads often resulting in delays in the delivery of shocks. Consequently we do not recommend a particular position for electrode placement over another.

A final point should be made about the use of antiarrhythmic drugs prior to attempted cardioversion. While evidence is limited, in patients who have been pretreated with amiodarone, ibutilide, propafenone or sotalol, the restoration of a sinus rhythm from AF required less electrical energy, fewer attempts and lower number of recurrences.15,16,17,18 Further studies however are required to determine if these findings are representative within the ICU population.

Pregnancy

Among the various cardiac pathologies complicating pregnancy, arrhythmias are the most common. Often diagnosed for the first time during pregnancy, tachyarrhythmias are the commonest form of arrhythmias reported during pregnancy. Cardioversion and defibrillation during pregnancy is relatively safe without documented adverse effects to the fetus. However, antepartum fetal monitoring is recommended to monitor fetal heart rate during the procedure. Special consideration of the duration of pregnancy should be made while choosing drugs used for sedation pre-procedure, for example, avoid midazolam. Positioning of patients in the left lateral position if possible also allows the patient to better tolerate the hemodynamic changes associated with cardioversion/defibrillation.

Since the implantation of the first ICD in 1980, there has been a great increase in the use of these instruments and their presence in ICU patients. Occasionally patients continue to have unstable tachyarrhythmias despite having a functioning device. In certain instances, the ICD can be successfully reprogrammed to deliver the shock internally or implement tachycardia-pacing strategies for managing tachyarrhythmia.

The application of electrical current during synchronized and unsynchronized cardioversion in patients with an ICD or permanent pacemaker can potentially cause damage to the ICD circuit and cause malfunction of these devices. However, hemodynamically unstable tachyarrhythmias that are not being controlled by the implanted device need to be treated without hesitation in a manner similar to any other patient in the ICU.

As a strategy for minimizing risk of device damage, it is recommended to place the pads at least 12 cm away from the pulse generator and to use the anteroposterior positioning of electrodes. All ICDs and permanent pacemakers should be interrogated after cardioversion is performed to ensure the proper functioning of these devices.

A common concern that is raised with the use of cardioversion refers to its use in patients on digoxin and the risk of post-cardioversion ventricular ectopy/arrhythmias. An initial study from 1966 revealed a significant increase in the incidence of serious postcardioversion ventricular ectopy in patients that had ECG evidence of digitalis toxicity precardioversion.19 This however was noted to occur most commonly in patients that received monophasic shocks with energy greater than 200 J. Subsequent studies have confirmed that sustained ventricular ectopy post cardioversion is exceedingly rare and tends to occur with higher energy cardioversion along with other concomitant factors such as hypokalemia. As with all tachyarrhythmias it is important to identify and treat the underlying cause. If cardioversion is deemed necessary it should be carried out starting with a lower energy level and ensuring the correction of any electrolyte abnormalities.

Complications of cardioversion include skin burns, transient hypotension (commonly from sedation), and EKG changes (such as nonspecific ST-T wave changes or transient ST segment elevation). High-energy shocks may also result in myocardial necrosis, which may present as a small rise in cardiac enzymes.20 In contrast acute myocardial ischemia causes significant elevations of cardiac enzymes and may not be directly related to cardioversion itself. Myocardial dysfunction may also occur due to myocardial stunning and is usually related to ischemia during cardiac arrest. This complication usually improves in 24 to 48 hours post resuscitation. Rarely, pulmonary edema may occur as a result of left atrial standstill or LV dysfunction after cardioversion in patients with longstanding AF.

The two most common potentially life-threatening complications associated with cardioversion and defibrillation are arrhythmia and thromboembolism. Arrhythmias include sinus tachycardia, non-sustained VT, bradycardia and occasionally complete heart block that may require temporary cardiac pacing. Clinically significant VT or VF may also occur infrequently. Previous studies in patients with atrial fibrillation have reported a post cardioversion stroke risk of 1.1% if anticoagulated for 3 weeks and 7% if not anticoagulated.21

Much of these studies are retrospective analyses of data from emergency room visits and their results have not been reproduced in the ICU setting. The benefits of cardioversion in unstable AF outweighs the risk of clot embolization and therefore, urgent synchronized cardioversion should not be delayed in these patients. The process of oxygenating at the time of delivery of shock has come under scrutiny as a result of the risk for potential arcing/sparks leading to a fire. Despite defibrillation being used for several decades there have been only 2 reported cases of fire as a result of cardioversion/defibrillation.22 We do not recommend any special precautions with regards to oxygenation and the delivery of electrical shocks.

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Capucci  A, Villani  GQ, Aschieri  D, Rosi  A, Piepoli  MF. Oral amiodarone increases the efficacy of direct-current cardioversion in restoration of sinus rhythm in patients with chronic atrial fibrillation. Eur Heart J. 2000;21:66–73.  [PubMed: 10610746]

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Lai  LP, Lin  JL, Lien  WP, Tseng  YZ, Huang  SK. Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes. J Am Coll Cardiol. 2000;5:1434–1441.

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Arnold  AZ, Mick  MJ, Mazurek  RP, Loop  FD, Trohman  RG. Role of prophylactic anticoagulation for direct current cardioversion in patients with atrial fibrillation or atrial flutter. J Am Coll Cardiol. 1992;19:851–885.  [PubMed: 1545081]

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Hummel  RS, Ornato  JP, Weinberg  SW,  et al. Spark-generating properties of electrode gels used during defibrillation. A potential fire hazard. J Am Med Assoc. 1988;260:3021–3024.