ACLS 2005 Ventricular Fibrillation (VF)/
Pulseless Ventricular Tachycardia (PVT) Algorithm
The following acronym directs AHA accepted actions after the Primary ABCDs have been enacted and an AED or Manual Defibrillator arrives and a shockable rhythm (VF or PVT) is present:
SCREAM
Letter Intervention Note
S Shock 360J* monophasic, 1st and subsequent shocks.(Shock every 2 minutes if indicated)
C CPR After shock, immediately begin chest compressions followed by respirations (30:2 ratio) for 2 minutes. (Do not check rhythm or pulse)
R Rhythm Rhythm check after 2 minutes of CPR (and after every 2 minutes of CPR thereafter) and shock again if indicated. Check pulse only if an organized or non-shockable rhythm is present.
Implement the Secondary ABCD Survey. Continue this algorithm if indicated. Give drugs during CPR before or after shocking. Minimize interruptions in chest compressions to <10 seconds. Consider Differential Diagnosis.
E Epinephrine 1 mg IV/IO q3-5 min. Or vasopressin 40 U IV/IO, once, in place of the 1st or 2nd dose of epi.
A
M Anitarrhythmic Medications Consider antiarrhythmics. (Any Legitimate Medication) Amiodarone 300mg IV/IO, may repeat once at 150mg in 3-5 min. if VF/PVT PERSISTS or Lidocaine (if amiodarone unavailable) 1.0-1.5 mg/kg IV/IO, may repeat X 2, q5-10 min. at 0.5-0.75 mg/kg, (3mg/kg max. loading dose) if VF/PVT persists,or Magnesium Sulfate1-2 g IV/IO diluted in 10mL D5W(5-20 min. push) for torsades de pointes or suspected/ known hypomagnesemia.
* Biphasic energy level is device dependent, follow the manufacturer's recommendation. If recommendation is unknown, use 200J for 1st shock and the same or higher energy level for subsequent shocks.
TREATMENT :
Defibrillation
External electrical defibrillation remains the most successful treatment of VF. A shock is delivered to the heart in order to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. The objectives are to interfere with all reentrant arrhythmia and to allow any intrinsic cardiac pacemakers to assume the role of primary pacemaker.
Successful defibrillation largely depends on 2 key factors: duration between onset of VF and defibrillation and the metabolic condition of the myocardium. VF waveform usually begins with a relatively high amplitude and frequency; it then degenerates to smaller and smaller amplitude until asystole after approximately 15 minutes, possibly from depletion of the heart's energy reserves. Consequently, early defibrillation is vital; emergency response teams can perform defibrillation before arrival at the ED.
Defibrillation success rates decrease 5-10% for each minute after onset of VF. Success rates of 85% have been reported in strictly monitored settings where defibrillation was most rapid.
Factors that increase the energy required for successful defibrillation include the following:
Time before defibrillation begins
Paddle size
Paddle-to-myocardium distance (eg, obesity, mechanical ventilation)
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, which decrease defibrillation threshold
The goal is to use the minimum amount of energy required to overcome the threshold of defibrillation. Excessive energy can cause myocardial injury and arrhythmias.
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. Position one paddle below the outer half of the right clavicle and one over the apex (V4-V5).
Artificial pacemakers or ICDs necessitate the use of anteroposterior paddle placement.
Before any defibrillation, remove all patches and ointments from the chest wall because they create a risk of fire or explosion.
Patient must be dry and not in contact with metallic objects. Rescuers must remember to ensure the safety of everyone around the patient before each shock is applied.
If contraction is reestablished following defibrillation, a period of low cardiac output (ie, postcountershock myocardial depression) may occur. Cardiac output recovery may take minutes to hours.
Defibrillation causes serum creatine phosphokinase levels 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 reference ranges unless an infarction has caused myocardial injury.
Although precordial thump is less appropriate for VF than for VT, it really is appropriate in neither. Use it only for witnessed monitored arrests in which no defibrillator is immediately available.
Algorithm
Activate emergency response system.
Initiate CPR.
Verify that the patient is in VF as soon as possible (ie, AED, quick look with paddles).
Defibrillate the patient (adult, 200 J; child, 2 J/kg or equivalent biphasic energy).
Defibrillate the patient (adult, 200-300 J; child, 2-3 J/kg or equivalent biphasic energy).
Defibrillate the patient (adult, maximum 360 J; child, 4 J/kg child; maximum biphasic energy varies with manufacturer).
Check for pulses/rhythm.
Perform CPR for 1 minute with attention to the following:
Properly positioning the electrode
Attempting tracheal intubation and IV access
Administering epinephrine every 3 minutes
Correct the following if necessary and/or possible:
Hypoxia
Hypovolemia
Hyperkalemia/hypokalemia and metabolic disorders
Tension pneumothorax
Tamponade
Toxic/therapeutic substances
Thromboembolic/mechanical obstruction
Defibrillate the patient (adult, 360 J; child, 4 J/kg or maximum biphasic).
Administer amiodarone (300 mg IV). If not available, use lidocaine (1-1.5 mg/kg bolus).
Defibrillate the patient (adult, 360 J; child, 4 J/kg or maximum biphasic).
Administer lidocaine (1 mg/kg IV) if amiodarone was used in the first round.
Other options are as follows: If not used in the first round, administer amiodarone (300 mg IV) now, and repeat lidocaine.
Administer amiodarone IV bolus only once.
Defibrillate the patient (adult, 360 J; child, 4 J/kg or maximum biphasic).
If no response, administer epinephrine 1 mg IV push or vasopressin (40 U IV push). Vasopressin can be used only once. Wait 10 minutes after vasopressin administration before giving epinephrine.
Administer a procainamide infusion (50 mg/min IV) to a total of 1 g.
Following the third shock, intervals between consecutive jolts should not exceed 1 minute.
Assess use of the following in conjunction with subsequent defibrillation attempts, and administer a shock 30 seconds after each dose of the indicated drug:
Lidocaine (1-1.5 mg/kg IV; maximum 3 mg/kg total)
Amiodarone (0.5 mg/min following bolus dosing above or IV loading protocol below)
Epinephrine (0.1-0.2 mg/kg IV): For adults, 1 mg IV every 3 minutes is typically used; alternative dosing regimens are advocated (ie, high, intermediate, escalating).
Procainamide (30 mg/min IV; maximum 17 mg/kg total in refractory VF)
Magnesium sulfate (1-2 g IV push) in cases of probable hypomagnesemia or refractory VF
Sodium bicarbonate (1 mEq/kg IV push) in cases of known preexistent hyperkalemia or known tricyclic antidepressant overdose
Three initial defibrillation attempts take precedence over CPR as soon as a defibrillator or AED is available.
Lidocaine and epinephrine can be administered through an endotracheal tube if IV attempts fail. Use 2.5 times the IV dose.
Refractory VF
Lack of response to standard defibrillation algorithms is challenging. Addition of magnesium and/or procainamide is often ineffective.
If not used earlier, consider the following amiodarone-loading protocol: 15 mg/min for 10 minutes, followed by 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours.
Such reported alternatives as transesophageal and intracardiac defibrillation or thoracotomy with internal defibrillation are generally impractical because of limited experience and availability of equipment and trained personnel.
Postresuscitative care
Continue successfully used antiarrhythmics. Maintain lidocaine at 1-4 mg/min, bretylium at 1-2 mg/min, and amiodarone at 0.5 mg/min.
Control any hemodynamic instability.
Administer vasopressors as indicated.
Postdefibrillation arrhythmias (mainly AV blocks) have been reported in up to 24% of patients. The incidence is related to the amount of energy used for defibrillation.
Check for complications (eg, aspiration pneumonia, CPR-related injuries).
Establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).
Medical stabilization: Careful postresuscitative care is essential to survival because studies have shown a 50% repeat in-hospital arrest rate for people admitted after a VF event. Treatment of myocardial ischemia, heart failure, and electrolyte disturbances are all justified by the results of multiple randomized trials investigating acute MI and CHF. Empiric beta-blockers are reasonable in many circumstances because of favorable properties discussed in Causes. Empiric antiarrhythmics, including amiodarone, should not supersede ICD placement unless control of recurrent VT is needed while the patient is hospitalized.
Surgical Care: Most survivors of VF should be treated with ICDs. Transvenous ICDs can be placed with minimal morbidity and mortality.
Radiofrequency ablation: Now routinely available, radiofrequency ablation is indicated for patients with AV bypass tracts, bundle-branch block VT, RVOT tachycardia, idiopathic LV tachycardia, and more rare forms of automatic foci VT (which almost never cause VF). Unfortunately, most cases of VF are not amenable to radiofrequency ablation and require ICD placement. VF is an exception because of preexcited tachycardias in patients with WPW syndrome. In these patients, successful catheter ablation of the accessory pathway(s) is the appropriate therapy.
Several multicenter trials have examined the prophylactic use of ICD therapy in patients at high risk for VF.
The annual VF rate in patients with these devices has been reduced from 25% to 1-2%. ICD placement is beneficial in high-risk patients in whom electrophysiologic-guided therapy with antiarrhythmics has failed. In several studies comparing ICD placement with antiarrhythmic therapy in patients with VT/VF and/or prior cardiac arrest, ICD placement has been shown to be associated with significantly decreased mortality rate (Myerburg, 1997; Cappato, 1999; Domanski, 1999).
The use of ICDs as primary prevention for VF is still being investigated in ongoing trials. Newer ICDs have pacing capabilities and have addressed bradyarrhythmias either causing or complicating VT or VF.
Currently, the transvenous approach to implantation is universally applied and favored over the thoracotomy implants. In the Multicenter Automatic Defibrillation Implantation Trial (MADIT) 1, prophylactic use of ICDs in patients with a history of MI, LVEF of less than 35%, documented episode of nonsustained VT, and inducible nonsuppressible VT had a 54% reduction in mortality during any follow-up interval compared with patients treated with conventional medical therapy. In MADIT 2, the ICD conferred a 31% reduction in mortality in patients with prior MI and LVEF of 30% or less. In MADIT 2, there was no requirement for nonsustained VT or EPS (Moss, 1996; Moss, 2002).
Cardiac surgery can be a primary treatment for VF via a variety of strategies.
Surgical treatment in patients with ventricular arrhythmias and ischemic heart disease includes coronary artery bypass grafting (CABG). The CASS study illustrated that patients with significant CAD and operable vessels who underwent CABG had a decrease in the incidence of VT/VF arrest compared with patients on conventional medical treatment. The reduction was most evident in patients who had 3-vessel disease and CHF (Holmes, 1989). By itself, CABG only prevents recurrent VF if the ejection fraction is normal and ischemia was the cause of the arrest. Even in these patients, ICDs are frequently placed after CABG.
Surgical treatment of ventricular arrhythmias in patients with nonischemic heart disease includes excision of VT foci after endocardial mapping and excision of LV aneurysms. This is practiced very infrequently, however, given the efficacy of ICDs.
Aortic valve replacement is associated with improved outcome in patients with hemodynamically significant valvular stenosis and well-preserved ventricular function. In patients with MVP associated with significant valvular regurgitation and LV dysfunction, malignant tachyarrhythmias, such as VT and VF, have been reported. These patients are candidates for mitral valve replacement.
Orthotopic heart transplantation is indicated in patients with SCD and refractory heart failure, in whom significant improvement in actuarial survival is expected. Given a limited donor service, this form of treatment is expected to be beneficial for very few people who survive VF.
Patients with long QT syndrome who do not respond to beta-blockers are candidates for ICD placement or high thoracic left sympathectomy.
DRUG THERAPY : Medications (eg, vasopressin, epinephrine, amiodarone) are used after 3 defibrillation attempts are performed to restore normal rhythm.
Amiodarone can also be used on a long-term basis in patients who refuse ICDs or who are not candidates for ICDs.
1. ANTIARRHYTHMIC AGENTS : CLASS I DRUGS ARE LESS EFFECTIVE THAN CLASS III AGENTS & SHOULD BE AVOIDED IN PATIENTS WITH STRUCTURAL HEART DISEASE
- AMIODARONE
- SOTALOL
- LIDOCAINE
- PROCAINAMIDE
- BETA BLOCKERS : TO TREAT ISCHAEMIA, AND AS PROPHYLAXIS IN CONGENITAL LONG QT SYNDROME
-MAGNESIUM SULPHATE
2. ANTICHOLINERGIC DRUGS : Improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade
- ATROPINE SULPHATE
3. VASOPRESSOR AGENTS :
- EPINEPHRINE
- VASOPRESSIN