Ventricular Fibrillation in Emergency Medicine

Ventricular fibrillation (VF) begins as a quasiperiodic reentrant pattern of excitation in the ventricles with resulting poorly synchronized and inadequate myocardial contractions. The heart consequently immediately loses its ability to function as a pump. As the initial reentrant pattern of excitation breaks up into multiple smaller wavelets, the level of disorganization increases. Sudden loss of cardiac output with subsequent tissue hypoperfusion creates global tissue ischemia; brain and myocardium are most susceptible. VF is the primary cause of sudden cardiac death (SCD).

Ventricular fibrillation is shown in the rhythm strip below.

Essential Update: COVID-19

Coronavirus disease 2019 (COVID-19) is defined as illness caused by a novel coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); it is known to spread through aerosolized particles produced by an infected person.[1] Emergency care personnel are at an increased risk of exposure owing to proximity to and aerosol-generating procedures performed on patients, such as intubation and CPR. The American Heart Association, in collaboration with seven other medical societies, has issued interim guidance to help rescuers treat adult and pediatric patients with cardiac arrest with suspected or confirmed COVID-19.[2, 3]

The Interim Guidance for Basic and Advanced Life Support in Adults, Children, and Neonates With Suspected or Confirmed COVID-19 includes detailed recommendations on life-saving interventions in the context of the COVID-19 pandemic, including the following:

• General principles for resuscitation in patients with suspected and confirmed COVID-19

• Algorithms with key updates to basic and advanced cardiovascular life support procedures for patients with suspected and confirmed COVID-19

• Situation- and setting-specific considerations, including out-of-hospital and in-hospital cardiac arrest as well as maternal and neonatal considerations for patients with suspected and confirmed COVID-19

See the guidelines for complete information.

Patient Education

For patient education information, see the Heart Health Center and Healthy Living Center, as well as Cardiopulmonary Resuscitation (CPR) and the National Library of Medicine's Ventricular Fibrillation.

Sudden cardiac death can be viewed as a continuum of electromechanical states of the heart: ventricular tachycardia (VT), ventricular fibrillation (VF), pulseless electrical activity (PEA), and asystole. VF is the most common initial state encountered, and, because of insufficient perfusion of vital cardiac tissues, it degenerates to asystole if left untreated.

The etiology of VF remains incompletely understood. It often occurs in the setting of acute cardiac ischemia or infarction, and acute myocardial infarction (MI) is diagnosed in up to half of sudden-death survivors. The incidence of sudden death is also relatively high in the postinfarction period for months after an MI. Abnormal rapid stimulation of the ventricles can lead to fibrillation. This can occur during VT or in conditions, such as Wolff-Parkinson-White syndrome, when atrial fibrillation or flutter waves pass rapidly through a bypass tract to the ventricular musculature. Severe left ventricular dysfunction, a variety of cardiomyopathies, and acquired or idiopathic long QT syndrome also increase the risk of fibrillation.

Multiple events may lead to the initiation of VF. One etiology is mechanical or electrical stimulation of the myocardium during the early phase of repolarization (termed R-on-T phenomenon). When an impulse is delivered to the heart during the time period that corresponds to the upslope of the T wave, the ventricular myocardium is in a variable state of excitability because some of the muscle is still partly or completely refractory. The impulse may propagate electrically through the tissue but at a decreased rate through a tortuous pathway. Slowed abnormal conduction may allow the wave of depolarization to circle around and reexcite areas that have had sufficient time for partial or complete repolarization. Areas that are activated again after partial repolarization may again exhibit abnormal slow propagation allowing sustained reentry and fibrillation.

Sustained VF may be due to a relatively small number of macroreentrant circuits or rotors, which are relatively stationary or drift through the 3-dimensional volume of the ventricular myocardium. These rotors may activate the cardiac muscle fibers at a high frequency, with secondary wavefronts emanating, traveling, and breaking up at variable distances from the source.

All fibrillation is not the same. VF begins as a coarse, irregular deflection on the ECG, then degenerates to a fine, irregular pattern, and eventually becomes asystole. This progression of electrocardiographic abnormalities reflects the electrical and energetic changes described above. The probability of successful defibrillation decreases as the VF waveform becomes smoother with time.[4]

Cardiac causes with structural heart disease include the following:

• Myocardial ischemia or infarction due to coronary artery disease: Coronary atherosclerosis and its consequences are responsible for approximately 80% of sudden cardiac deaths in the United States.

• Cardiomyopathy: Dilated and hypertrophic cardiomyopathies are the second most important cardiac causes of sudden death. The degree of functional and physiologic left ventricular impairment is correlated with the risk of sudden death: dilated, hypertrophic, or arrhythmogenic right ventricular cardiomyopathy or dysplasia.

• Aortic stenosis

• Aortic dissection

• Pericardial tamponade

• Congenital heart disease

• Myocarditis

Cardiac causes in the absence of structural heart disease include the following

• Catecholaminergic polymorphic ventricular tachycardia and right ventricular outflow tract tachycardia

• Mechanical (commotio cordis)[5] or electrical accidents

• Preexcitation (including Wolff-Parkinson-White syndrome)

• Heart block

• Drug-induced QT prolongation with torsades de pointes

• Channelopathies: long QT syndrome, short QT syndrome, or Brugada syndrome[6]

Noncardiac respiratory causes include the following:

• Bronchospasm

• Aspiration

• Sleep apnea

• Primary pulmonary hypertension

• Pulmonary embolism

• Tension pneumothorax

Metabolic or toxic causes include the following:

• Electrolyte disturbances and acidosis

• Medications or drug ingestion

• Environmental poisoning

• Sepsis

Neurologic causes include the following:

• Seizure

• Cerebrovascular accident - Intracranial hemorrhage or ischemic stroke

• Drowning

United States data

The incidence of sudden cardiac death in the United States is approximately 300,000 cases per year. The distribution of rhythms found in patients with cardiac arrest depends largely on the average duration of the arrest state and, thus, the emergency medical system (EMS) response times. In monitored settings, such as casinos, where average response times are less than 5 minutes, the initial rhythm is ventricular fibrillation (VF) in approximately 70% of patients.[7] A circadian pattern of sudden cardiac death has also been reported.

The incidence of VF seems to be decreasing based on multiple reports. This may, in part, be due to improved treatment of coronary artery disease and acute myocardial infarction, implantable cardioverter-defibrillator (ICD) placement in patients at high risk,[8] or other unknown factors.

International data

Ventricular fibrillation also is prevalent worldwide, with a reported predominance in the northern hemisphere. Among some European populations, the annual incidence of cardiac arrests exceeds 6 cases per 10,000 people.

Race-, sex-, and age-related demographics

Black males have the highest incidence of sudden cardiac death.

Sudden cardiac death is more common among males than females, although the rates become similar for patients older than 70 years.

Incidence of sudden cardiac death initially peaks during the first 6 months of life, then rapidly declines until a second peak in those aged 45-75 years.

The prognosis for survivors of ventricular fibrillation (VF) strongly depends on the time elapsed between onset and medical intervention. Early defibrillation often makes the difference between long-term disability and functional recovery.

The likelihood of survival of cardiac arrest victims also depends on the duration of arrest prior to treatment. Improved outcomes occur in patients who have a witnessed arrest, receive bystander cardiopulmonary resuscitation (CPR), obtain defibrillation and advanced cardiac life support from EMS personnel within 10 minutes of onset, and present with an initial rhythm of VF.[6]

Cardiac arrests witnessed by bystanders have a better prognosis because the victim is more likely to receive early treatment. The rate of survival from VF in the community varies from 4-33%. The survival rate of all cardiac arrest victims regardless of presenting rhythm has been reported to be as high as 18% and as low as 2% in various EMS systems. Large urban centers tend to have lower rates of survival. These lower rates of survival have been attributed to lower rates of bystander CPR, longer response intervals, and fewer patients presenting with VF.[9]

Morbidity/mortality

Postresuscitation death and disability after successful resuscitation directly correlate with the degree of central nervous system (CNS) damage during the event. Without intervention, by 4-6 minutes after onset of VF, the prognosis is poor. Few survive when VF lasts more than 8 minutes without intervention. Prediction rules have been developed to predict favorable neurologic survival from cardiac arrest.[10, 11]

The reported rate of survival from VF in the community varies from 4-33%. Survival is worst in dense urban and sparse rural areas, principally due to prolonged EMS response times.

Cardioverter-defibrillator implantation is the primary treatment of survivors of VF. Antidysrhythmic and beta-adrenergic blocking medicines may also be helpful to prevent VF recurrence. While these interventions lower the risk of sudden dysrhythmic death, the implantable cardioverter-defibrillator (ICD) in particular does not prevent or retard the progressive congestive heart failure that is often present in these patients.

Complications

Complications of ventricular fibrillation include the following:

• CNS ischemic injury

• Myocardial injury

• Postdefibrillation arrhythmias

• Aspiration pneumonia

• Defibrillation injury to self or others

• Injuries from CPR and resuscitation

• Skin burns

• Damage to implanted electronics (eg, ICD, pacemaker)

• Death

Ventricular fibrillation (VF) often occurs without forewarning. The following symptoms, while not necessarily specific for sudden cardiac death or VF, may develop before any major cardiac event:

• Chest pain and other angina equivalents

• Dyspnea

• Easy fatigue

• Palpitations

• Syncope

• Immediately preceding acute cardiac arrest, possible increase in heart rate, presence of premature ventricular contractions (PVCs), or period of VT

Physical examination findings may include no pulse or respiration as well as wide and chaotic QRS complexes on cardiac monitors.

Patients in cardiac arrest have no pulse. However, both lay rescuers and healthcare providers may have difficulty determining pulselessness. Current AHA guidelines do not recommend that lay rescuers check for a pulse. Healthcare providers should take no more than 10 seconds to check for a pulse. If no pulse is found, the provider should proceed with chest compressions.

Patients in cardiac arrest have absent or abnormal (gasping) respirations. Adults who are unresponsive or have been witnessed to collapse, and have absent or abnormal respirations are likely to be in cardiac arrest. AHA guidelines recommend activating the emergency response system (call 911) and initiating CPR.

Patients in cardiac arrest become unconscious.

Laboratory studies in the workup of ventricular fibrillation include the following:

• Serum electrolyte levels, including calcium and magnesium

• Cardiac enzymes to identify myocardial injury

• Complete blood count (CBC) to detect contributing anemia

• Arterial blood gases (ABGs) and serum lactate levels to assess the degree of acidosis or hypoxemia

• Toxicologic screens and levels as clinically indicated

Chest radiography may identify aspiration pneumonia, pulmonary edema, cardiomegaly, and injury (eg, secondary to cardiopulmonary resuscitation [CPR]).

Electrocardiography (ECG) is used to help identify ischemic or proarrhythmic conditions.

Because of the critical importance of early defibrillation, prehospital care is vital for arrests due to ventricular fibrillation (VF) that occur outside the hospital.

Interventions that impact survival and outcome of resuscitation include the following:

• Witnessed or early recognition of an arrest

• Early activation of emergency medical services (EMS) system

• Bystander CPR slows the degeneration of VF and improves survival.

• Automated external defibrillator (AED) application and defibrillation by trained personnel in the field

• Early access to trained EMS personnel capable of performing CPR, defibrillation, and advanced cardiac life support (ACLS)

Bystander CPR

Traditionally, CPR consists of artificial respirations and chest compressions. Mounting evidence demonstrates that high quality chest compressions are the critical action to provide some cardiac perfusion during CPR, and artificial respirations are less important.[16, 17, 18, 19] Interruption of chest compressions to perform artificial respirations by a single resuscitator causes a loss of cardiac perfusion pressure, and even after restarting compressions, it may take some time before the previously obtained perfusion pressure is restored.

Other concerns exist regarding the recommendation of artificial ventilations routinely for VF arrest. Rescuers may be prone to hyperventilate the victim, which may lead to increased intrathoracic pressure, and resulting decreased coronary perfusion and survival.[20] Bystanders may be more likely to perform CPR that involves only chest compressions and no artificial respirations.

Current American Heart Association (AHA) guidelines recommend immediate treatment with 30 chest compressions prior to any artificial ventilations.

Untrained lay rescuers should continue to provide chest compressions only with an emphasis on "push hard and fast." This should continue until an AED arrives or healthcare providers are ready to take over care.

Trained lay rescuers should provide 30 compressions to 2 artificial breaths.

Healthcare providers should perform cycles of 30 chest compressions to 2 ventilations until an advanced airway is placed. After that, chest compressions can be performed continuously along with provision of one breath every 6 to 8 seconds.

AHA guidelines reflect developments in this ongoing area of research, including the "cardiocerebral resuscitation" approach, also summarized after the AHA algorithm (see Emergency Department Care).[21] This approach emphasizes minimal interruption of continuous chest compressions (CCC) for victims of witnessed cardiac arrest.  More recent data do not suggest a difference in outcome between performance of CPR by EMS providers with chest compressions that are continuous or interrupted by artificial ventilations.[22]

It is important to note the arguments above apply to the use of artificial respirations for initial resuscitation of VF circulatory arrest. Future research may confirm the importance of artificial respirations for respiratory, drowning, traumatic, or other causes of arrest. It is becoming clear that the optimal treatment for these conditions with grossly different etiologies will differ and "one size will not fit all."

Automated external defibrillator (AED) application and defibrillation by trained personnel in the field

AEDs have revolutionized prehospital VF management because they decrease the time to defibrillation. This is accomplished by having the units prepositioned in the field where cardiac arrests are likely to occur (eg, airports, casinos, jails, malls, stadiums, industrial parks), eliminating the need for rhythm-recognition training and increasing the number of trained personnel and laypeople that can defibrillate at the scene.

Unfortunately, even for a group of patients at high risk for VF/VT, placement of an AED in the home was not associated with improved mortality.[23] AEDs were also unhelpful in the hospital setting where early access to a manual defibrillator and trained personnel are available. They may even be detrimental to the resuscitation and survival of patients with nonshockable rhythms such as pulseless electrical activity and asystole.[24, 25]

AEDs are programmed to recognize three shockable rhythms: coarse ventricular fibrillation, fine ventricular fibrillation, and rapid ventricular tachycardia. Modern units have a sensitivity greater than 95% and specificity approaching 100% for the three shockable rhythms. The greatest difficulty is in distinguishing fine ventricular fibrillation from asystole.

AEDs can also be used for children. A pediatric dose-attenuating system should be used, if available, for children up to the age of 8 years, and a conventional AED can be used for children at or older than 8 years or with a corresponding weight of at least 25 kg (55 lb).

Defibrillation

Electrical external defibrillation remains the most successful treatment of ventricular fibrillation (VF). A shock is delivered to the heart to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. The objective is to interfere with all reentrant arrhythmia and to allow any intrinsic cardiac pacemakers to assume the role of primary pacemaker.[26]

Successful defibrillation largely depends on the following two key factors: duration between onset of VF and defibrillation, and metabolic condition of the myocardium. VF begins with a coarse waveform and decays to a fine tracing and eventual asystole. These electrical changes that occur over minutes are associated with a depletion of the heart's energy reserves. CPR slows the progression of these events, but defibrillation is the primary treatment to interrupt the process and return the heart to a perfusing rhythm.

Defibrillation success rates decrease 5-10% for each minute after onset of VF. The likelihood of defibrillation success can also be predicted based on the smoothness of the VF tracing. In strictly monitored settings where defibrillation was most rapid, 85% success rates have been reported.

Factors that affect the energy required for successful defibrillation include the following:

• Paddle size: Larger paddles result in lower impedance, which allows the use of lower energy shocks. Approximate optimal sizes are 8-12.5 cm for an adult, 8-10 cm for a child, and 4.5-5 cm for an infant.

• Paddle-to-myocardium distance (eg, obesity, mechanical ventilation): Position one paddle below the outer half of the right clavicle and one over the apex (V4-V5). Artificial pacemakers or implantable defibrillators mandate use of anterior-posterior paddle placement.

• Use of conduction fluid (eg, disposable pads, electrode paste/jelly)

• Contact pressure

• Elimination of stray conductive pathways (eg, electrode jelly bridges on skin)

• Previous shocks may lower the chest wall impedance and decrease the defibrillation threshold.

Biphasic defibrillation

Biphasic defibrillation has a number of advantages over monophasic defibrillation including increased likelihood of defibrillation success for a given shocking energy.[27] While this has not translated into a proven survival benefit thus far, if less shocks are required, there may be less interruption of CPR. Lower energy shocks associated with biphasic defibrillation may lead to less myocardial stunning after repeated defibrillation attempts. Furthermore, smaller and lighter defibrillation units are required to produce a biphasic waveform, and this is an important advantage for portable AED units.

The optimal energy for first and subsequent defibrillation attempts with a biphasic pulse remains unproven. Escalating energy levels have been associated with increased VF conversion and termination. Unfortunately, no improvement in survival was noted.[28]

Operators are advised to use the energy protocols associated with individual devices, or to begin with 200 J and consider escalating energy dose with subsequent shocks, if necessary.

Predefibrillation Safety

Rescuers must remember to ensure the safety of everyone around the patient before each shock is applied. Prior to any defibrillation, remove all patches and ointments from the chest wall because they create a risk of fire or explosion. The patient must be dry and not in contact with metallic objects.

Goal

The goal is to use the minimum amount of energy required to overcome the threshold of defibrillation. Excessive energy may cause myocardial injury.

Defibrillation causes the serum creatine phosphokinase level to increase proportionate to the amount of electric energy delivered.

If customary voltage is used to defibrillate a patient, the proportion of myocardial fraction (CK-MB) should remain within normal limits unless an infarction has caused myocardial injury.

Postcountershock myocardial depression

If contraction is reestablished following defibrillation, a period may occur of low cardiac output, termed postcountershock myocardial depression. Cardiac output recovery may take minutes to hours.

CPR is important immediately after shock delivery. Many victims demonstrate asystole or pulseless electrical activity (PEA) for the first several minutes after defibrillation. CPR can convert these rhythms to a perfusing rhythm.

Provision of immediate CPR post defibrillation is a change included in the new AHA algorithm below.

"Priming the pump" predefibrillation CPR

Patients with VF for 4-5 minutes or more at the time defibrillation becomes available may benefit from a 1- to 3-minute period of CPR prior to initial defibrillation. The theoretical benefit of this intervention is "to prime the pump" by restoring some oxygen and other critical substrates to the myocardium to allow successful contraction post defibrillation. The clinical benefit of this intervention remains uncertain, but it has now been included as an optional protocol for Emergency Medical Services (EMS) in the AHA ACLS guidelines.[18, 29, 30]

AED units that can analyze the smoothness of the VF waveform are now available. These units essentially estimate the duration of fibrillation and likelihood of defibrillation success and advise immediate CPR or defibrillation depending on the reading.

Unfortunately, an initial EMS study using VF waveform analysis to guide the decision for initial therapy with immediate defibrillation or 2 minutes of CPR demonstrated no significant survival benefit over standard immediate defibrillation therapy.[31]

Precordial chest thump has been studied in a number of case series for patients in pulseless VT and VF. It has been found to convert VT and VF to a perfusing rhythm in some cases, but it has also been reported to accelerate VT, and to convert VT to VF and VF to asystole in other cases. This intervention is no longer routinely recommended.[32]

AHA Algorithm

The following summarizes the AHA algorithm[18] :

• Activate emergency response system.

• Initiate CPR and give oxygen when available.

• Verify patient is in VF as soon as possible (ie, AED and quick look with paddles).

• Defibrillate once: For adults, use a device specific or 200 J for biphasic waveform and 360 J for monophasic waveform; for children, 2 J/kg

• Resume CPR immediately without pulse check and continue for 5 cycles. One cycle of CPR equals 30 compressions and 2 breaths; 5 cycles of CPR should take roughly 2 minutes (compression rate 100 per minute). Do not check for rhythm/pulse until 5 cycles of CPR are completed.

• During CPR, minimize interruptions while securing intravenous access and performing endotracheal intubation. Once the patient is intubated, continue CPR at 100 compressions per minute without pauses for respirations, and administer respirations at 8-10 breaths per minute.

• Check rhythm after 2 minutes of CPR.

• Repeat a single defibrillation if still VF or pulseless VT with rhythm check. Use the same dose as the initial defibrillation for adults, and use 4 J/kg for this and all subsequent defibrillations for children.

• Resume CPR for 2 minutes immediately after defibrillation.

• Continuously repeat the cycle of (1) rhythm check, (2) defibrillation, and (3) 2 minutes of CPR

• Administer vasopressor: Give vasopressor during CPR before or after shock when intravenous or intraosseous access is available. Administer epinephrine 1 mg every 3–5 minutes. Consider administering vasopressin 40 units once instead of the first or second epinephrine dose.

• Administer antidysrhythmics. Give antidysrhythmic during CPR before or after shock. Administer amiodarone 300 mg IV/IO once, then consider administering an additional 150 mg once. Instead of or in addition to amiodarone, administer lidocaine 1-1.5 mg/kg first dose, then additional 0.5 mg/kg doses up to a maximum total of 3 mg/kg.

• If there is undulating polymorphic ventricular tachycardia suggestive of torsades de pointes (TdP), administer 1-2 g magnesium IV/IO.

• Administer sodium bicarbonate 1 mEq/kg IV/IO in cases of known or suspected preexistent hyperkalemia or tricyclic antidepressant overdose.

• Lidocaine and epinephrine can be administered through the endotracheal (ET) tube if IV/IO attempts fail. Use 2.5 times the IV dose.

In addition, correct the following if necessary and/or possible:

• Hypovolemia

• Hypoxia

• Hydrogen ion (acidosis) - Consider bicarbonate therapy.

• Hyperkalemia/hypokalemia and metabolic disorders

• Hypoglycemia (Check fingerstick or administer glucose.)

• Hypothermia (Check core rectal temperature.)

• Toxins

• Tamponade, cardiac (Check with ultrasonography.)

• Tension pneumothorax (Consider needle thoracostomy.)

• Thrombosis, coronary or pulmonary - Consider thrombolytic therapy if suspected.

• Trauma

Refractory or recurrent VF

Lack of response to standard defibrillation algorithms is challenging.

After initial amiodarone bolus, consider continued amiodarone therapy with 1 mg/min IV for 6 hours, then 0.5 mg/min for 18 hours.

If ongoing ischemia is the suspected cause of recurrent VF, consider emergent cardiac catheterization and possible angioplasty even in the absence of STEMI, and intra-aortic balloon pump placement.

For patients with prolonged and refractory in-hospital cardiogenic arrest that included VF/VT, it has been shown that extracorporeal cardiopulmonary resuscitation was associated with improved neurologically intact survival.[33] This study was performed in a large tertiary center with an ongoing protocol for this advanced experimental care.

Postresuscitative care

Antidysrhythmics used successfully should be continued. Maintain amiodarone at 0.5-1 mg/min and lidocaine at 1-4 mg/min.

Control any hemodynamic instability by administering vasopressors as indicated.

Check for complications (eg, aspiration pneumonia, CPR-related injuries).

Establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).

Cardiocerebral resuscitation

"Cardiocerebral resuscitation" is the term used to describe one cutting edge method for resuscitation that has yielded an improvement in survival.[21, 34] Based on the latest resuscitation research for all phases of resuscitation, the three pillars of this approach can be summarized as follows:

1. Cardiopulmonary resuscitation without mouth-to-mouth ventilations, or continuous chest compressions (CCC), for all patients with witnessed cardiac arrest.

2. EMS to administer 200 CCC before and after a single defibrillation for patients with arrest for greater than 5 minutes (circulatory phase of arrest[35] ). Cycle to be repeated three times prior to endotracheal intubation. Epinephrine to be given as soon as intravenous or intraosseous access available.

3. Postresuscitation care to include targeted temperature management particularly to avoid hyperthermia, although the ideal hypothermic target remains uncertain.[36] Urgent cardiac catheterization including percutaneous coronary intervention as needed, unless it is otherwise contraindicated.

Consultations

Consult a cardiologist or intensivist for continued inpatient ICU care.

Resuscitated patients must be admitted to an intensive care unit and monitored because of high risk of a recurrence. They require stabilization and monitoring for possibility of a coexistent emergency or complication.

Evaluation of ischemic injury to the CNS, myocardium, and other organs is essential.

Patients typically have an underlying etiology that must be investigated and treated.

Up to approximately half of cardiac arrest survivors have evidence of an acute MI. Both emergent thrombolytic therapy and percutaneous transluminal coronary angioplasty (PTCA) have been used to treat these patients; however, CPR for greater than 10 minutes is considered a relative contraindication to thrombolysis. Furthermore, thrombolytic therapy has not proven beneficial when administered unselectively to all cardiac arrest patients.[37] Cardiology consultation is warranted for all survivors of cardiac arrest, and efforts at revascularization should be attempted selectively, as indicated.[38, 39]

Patients who remain comatose post resuscitation may benefit from 12-24 hours of controlled hypothermia therapy at 32-34 degrees Centigrade (89.6-93.2 degrees Fahrenheit) or at least euthermia and avoidance of fever. Hypothermia can be accomplished with chemical sedation and paralysis to prevent shivering and an external cooling blanket or ice. Hypothermia therapy improved both neurologic outcome and mortality in two initial trials, but this result was not observed in a more recent study.[36, 40, 41]

Implantable cardioverter-defibrillator (ICDs) are recommended for patients at risk for recurrent VF because they effectively provide early defibrillation. Patients with VF arrest who receive ICDs have improved survival compared with those receiving only medications. However, patients with ICDs may also require oral antidysrhythmic therapy to minimize recurrent device activation.

In the setting of acute myocardial infarction, beta-adrenergic blocking therapy with agents such as metoprolol decrease the likelihood of ventricular dysrhythmias including ventricular fibrillation, and they lower overall mortality. Consider administering a beta-adrenergic blocking agent during acute myocardial infarction unless contraindicated by bradycardia, heart block, congestive heart failure, or reactive airway disease.

Treatment goals are to electrically terminate ventricular fibrillation (VF) so that an organized electrical rhythm follows and restores cardiac output. Success rates significantly decrease as the duration of ischemia increases. Drug therapy to facilitate defibrillation may consist of vasopressors, antidysrhythmics, electrolytes, and other agents.

The theoretical benefit of vasopressor medicines, such as epinephrine and vasopressin, is that they increase coronary perfusion pressure. Coronary perfusion pressure is the difference between aortic and right atrial pressure during the relaxation phase of CPR, and it determines myocardial blood flow. Higher levels of coronary perfusion pressure are associated with increased survival in animal models of VF arrest.

Vasopressors, such as epinephrine, increase coronary perfusion pressure; however, no vasopressors have been proven to increase survival in humans. Nevertheless, they are recommended due to possible benefit. Epinephrine, 1 mg, is recommended every 3-5 minutes once IV or IO access is established, and vasopressin, 40 units, may be administered once instead of the first or second epinephrine dose. Higher doses of epinephrine, 0.1-0.2 mg/kg, have been studied, but they are not clearly beneficial compared with the standard 1-mg dose.[42]  Data suggest no synergistic effect of administering vasopressin in addition to epinephrine.[43, 44]

Antidysrhythmic agents are recommended when initial defibrillation and vasopressor medicines fail or after successful defibrillation to prevent recurrence. Potential benefits of antidysrhythmic therapy include lowering the threshold for defibrillation and preventing immediate or delayed VF recurrence. Potential risks of antidysrhythmic therapy include hypotension due to decreased myocardial contractility or vascular tone, bradycardia, or asystole. No antidysrhythmic agent has been proven to improve survival to hospital discharge from VF arrest, but amiodarone may increase the likelihood of at least temporarily regaining a perfusing rhythm.[45, 46]

The mechanism of action of most antidysrhythmic agents is to alter the conductance of ions, such as sodium and potassium, across myocardial cell membrane ion conducting channels. Amiodarone and other Vaughn-Williams class III agents decrease the repolarizing flow of potassium across the cell membrane and cause a prolongation of the depolarized period. The cell is refractory to further excitation during this period and may not be able to conduct the VF waveform, thus breaking the reentrant cycle of excitation. Other class III agents that have been studied in cardiac arrest include bretylium and sotalol, but they have not been consistently shown to provide benefit.[47, 48]

Lidocaine is a Vaughn-Williams class IB agent that alters the depolarizing flow of sodium across the cell membrane and may be particularly effective in an ischemic or acidotic environment. Procainamide is a Vaughn-Williams class IA agent that affects both sodium and potassium flow across the cell membrane and may also rarely be used for refractory or recurrent VF.

Additional alternative medications include magnesium sulfate, propranolol, and sodium bicarbonate. Magnesium may be particularly important in stabilizing the cell membrane and in preventing after-depolarizations that are important in the genesis of torsades de pointes. Propranolol or other beta-adrenergic blocking agents may have a calming effect on the myocardium for patients with recurrent persistent VF often described as VF storm. Bicarbonate is useful to block the effects of tricyclic antidepressant overdose, to treat hyperkalemia that may be causing ventricular dysrhythmias, or to treat acidosis associated with prolonged cardiac arrest.

Class Summary

Augment both coronary and cerebral blood flow present during low-flow state associated with CPR.

Epinephrine (Adrenalin)

Increases coronary perfusion pressure but has not been proven to increase survival in cardiac arrest.

Vasopressin (Pitressin)

A nonadrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction. Its effects on outcome have not been proven to differ from epinephrine in VF arrest. It may be used instead of the first or second dose of epinephrine during cardiac arrest resuscitation. Since it lasts longer than epinephrine, vasopressin is used only once.

Class Summary

These agents alter electrophysiologic mechanisms responsible for dysrhythmia.

Lidocaine (Xylocaine, Dilocaine)

Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue.

Amiodarone (Cordarone)

Acute actions after IV bolus are to inhibit AV conduction and prolong the AV refractory period; IV amiodarone usually causes a decrease in systemic vascular resistance with coronary and peripheral vasodilatation and variable depressant effects on cardiac contractility. Eventually amiodarone lengthens the duration of repolarization (QT interval corrected for pulse rate) and refractory period in most cardiac tissue. Amiodarone improves the return of spontaneous circulation from VF arrest by uncertain mechanisms, but it has not been shown to improve survival to hospital discharge. When administered chronically, multiple other effects occur on adrenergic tone, thyroid function, and other systems.

Bretylium

Class III antidysrhythmic agent previously used for VF refractory to defibrillation, epinephrine, and lidocaine. Bretylium may increase the fibrillation threshold and ventricular myocardial refractory period by decreasing potassium conductance. Has catecholamine-releasing properties and adverse effects and is not used as initial treatment. Currently not commercially available in the United States.

Procainamide (Procanbid)

Vaughn-Williams class IA antidysrhythmic that blocks both sodium and potassium conducting channels. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity, and it widens the QRS interval. Procainamide also increases the refractory period of atria and ventricles with associated lengthening of the QT interval. Procainamide is used to treat both supraventricular and ventricular dysrhythmias.

Class Summary

These agents are considered therapeutic alternatives for refractory VF. Patients with persistent or recurrent VF following antidysrhythmic administration should be assessed for underlying electrolyte abnormalities as a cause for their refractory dysrhythmia. Among electrolyte abnormalities associated with VF are hyperkalemia, hypokalemia, and hypomagnesemia. Magnesium sulfate, calcium chloride, and sodium bicarbonate are used in VF secondary to other medications. Magnesium sulfate acts as an antidysrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VF caused by hyperkalemia.

Magnesium sulfate

Deficiency in this electrolyte is associated with SCD and can precipitate refractory VF. Magnesium supplementation is used to treat torsade de pointes, known or suspected hypomagnesemia, or severe refractory VF.

Sodium bicarbonate (Neut)

Only when the patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, tricyclic antidepressant, or phenobarbital overdose. Routine use not recommended.

Calcium chloride

Useful in treatment of hyperkalemia, hypocalcemia, or calcium channel blocker toxicity. Moderates nerve and muscle performance by regulating the action potential excitation threshold.