Cardiovascular 5: Ventricular Fibrillation/
Pulseless Ventricular Tachycardia Portal
The majority of patients who experience sudden cardiac arrest are initially in ventricular fibrillation (VF). VF has the greatest chance of all the cardiac arrest rhythms of being successfully treated, provided that the patient receives early treatment with electricity (defibrillation) accompanied by appropriate intervention with the American Heart Association chain of survival. Although some medications may help facilitate the conversion of VF/ventricular tachycardia (VT) to a perfusing rhythm, the early and repeated (if necessary) use of defibrillation shocks is the key to successful resuscitation of a patient in VF/VT and is the single greatest determinant of survival.1
See Ventricular Fibrillation/Pulseless Ventricular Tachycardia Algorithm
Defibrillation
To be successful in converting VF/VT to a perfusing rhythm, defibrillation must completely depolarize the myocardium, producing a temporary asystolic state. This provides the intrinsic myocardial pacemakers the opportunity to resume an organized rhythm.
While early defibrillation is always the highest priority in VF/VT arrest, the sequence of interventions may vary somewhat with the specific circumstances:
In the unmonitored hospital patient who goes into witnessed cardiac arrest, assessment for a shockable rhythm and immediate defibrillation with an AED or manual defibrillator are the highest priorities; however, if a defibrillator is not immediately available, CPR should be instituted until a defibrillator arrives.
In the unmonitored hospital patient who is found in unwitnesssed arrest, the priorities remain the same. However, a period of 1 to 3 minutes of CPR prior to defibrillation has been found to be possibly beneficial in out-of-hospital patients with more than 4 minutes of down time,2 and may be applicable under these circumstances as well.
In the monitored patient who goes into VF, immediate defibrillation is the treatment of choice. Under these circumstances only, if a defibrillator is not immediately available, a precordial thump may be effective.2
Energy Selection for Defibrillation
Many newer defibrillators (manufactured after the year 2000) produce a biphasic instead of a monophasic waveform. This achieves more consistent defibrillation at lower energy levels than was the case with older monophasic defibrillators. However, a variety of biphasic waveforms are in use, and each brand of defibrillator has its own recommended defibrillating energy. Some biphasic defibrillators are made to deliver the first shock at 120 J and do not escalate, while others start at 150 J and escalate to 200 J. Many devices will default to their initial defibrillation energy when the defibrillator function is activated. While the AHA has recommended all defibrillators indicate recommendations on the surface of the device, this is not consistently applied. Ideally, consult the manufacturer’s manual at time of purchase and clearly indicate the recommendations in some visible place on the device. In the absence of specific knowledge regarding energy levels recommended for the device, the following are reasonable guidelines3:
Adult defibrillation with known biphasic
defibrillator, or if
waveform (mono- or biphasic) is unknown: Maximum energy setting.
Adult defibrillation with known monophasic
defibrillator: 360 J for
the first and all subsequent shocks.
PEDS: Using either type of defibrillator, defibrillating dose is 2 J/kg for the first shock and 4 J/kg for subsequent shocks.1
Timing of Defibrillation With CPR
Prior to 2005, the recommended sequence of events once a defibrillator was available was to defibrillate up to 3 times in rapid succession if the patient remained in VF/VT. Current recommendations are to deliver the first shock, then immediately resume CPR for 5 cycles (or about 2 minutes) before re-assessing rhythm and pulse. This recommendation is based on the much higher first-shock success rate of biphasic devices combined with a recognized need to avoid long interruptions in CPR.1
Special Considerations of the Use of Electric Shocks With Ventricular Tachycardia
- Treat pulseless VT the same as VF.
- Treat sustained monomorphic VT associated with angina, pulmonary edema, or hypotension (BP < 90 mm Hg) with a synchronized electric shock of 100 J initial energy (biphasic or monophasic). Increasing energies may be used if not initially successful.
- Treat sustained monomorphic VT not associated with angina, pulmonary edema, or hypotension (BP < 90 mm Hg) according to the Ventricular Tachycardia Algorithm. See Vol I Acute Care Portals).
- Treat polymorphic VT as VF in patients in cardiac arrest or cardiovascular collapse. Treat with magnesium 1 to 2 grams IV/IO over 5 to 60 minutes if the patient is more stable and the rhythm appears to be torsades de pointes.
Medications Used in Ventricular Fibrillation/Pulseless Ventricular Tachycardia
The use of andrenergic agents, antiarrhythmic agents, and buffer therapy previously used extensively for the treatment of both VF and pulseless VT has been relegated to secondary roles. Review of randomized clinical trials has failed to confirm a benefit to the use of the time-honored medications, including epinephrine, lidocaine, amiodarone, procainamide, and buffer agents. This is not to indicate that medications listed in this portal should not be used during attempted resuscitation, but rather that the primary focus during resuscitation must be to use defibrillation early (and repeatedly if needed), manage the patient’s airway and ventilation, and seek causes for the cardiac arrest that can be successfully treated.
The following is a short review of medications that may be considered for use during the resuscitation efforts for a patient with VF/VT. See Ventricular Fibrillation/Pulseless Ventricular Tachycardia Algorithm.
A. Epinephrine (Class IIb recommendation)
Epinephrine has been for many years the first choice for treatment of patients in cardiac arrest, including VF/VT. Epinephrine does not act as an anti-fibrillatory drug but rather promotes its positive effects by stimulating the adrenergic receptors to increase cerebral and coronary blood flow, thus helping to prevent cerebral ischemia and rendering the heart more receptive to defibrillation by a converting shock.
Dosage:
1 mg IV push (10 mL of 1:10 000 epinephrine); may repeat
every 3 to 5
minutes if needed. ET Dose = 2-2.5 mg for adults (2-2.5 mL of 1:1000
preparation)
PEDS: Epinephrine 0.01 mg/kg
IV/IO (0.1 cc/kg of 1: 10 000 preparation)
or ET 0.1 mg/kg (0.1 cc/kg of 1:1000 preparation)
B. Vasopressin (Class indeterminate recommendation)
The
vasopressor agent for defibrillation refractory VF/pulseless VT can be
either epinephrine or vasopressin. As a vasoconstrictor, vasopressin
appears as effective as epinephrine, with fewer negative effects on the
heart.4
PEDS: No recommendation for
vasopressin
Dosage: Vasopressin dosage is recommended as a single dose of 40 units given IV push. Vasopressin has a 10 to 20 minute half-life as opposed to the 3 to 5 minute half-life of epinephrine. If the patient remains in VF/VT after the vasopressin, the recommendation is to give epinephrine 1 mg IV every 3 to 5 minutes starting 10 to 20 minutes after the dose of vasopressin.2
C. Amiodarone (Class IIb recommendation for VF/pulseless VT)
Amiodarone is now considered the drug of choice to use in shock-resistant VF/pulseless VT after the use of epinephrine/vasopressin.4,5 The administration of amiodarone may require several time-consuming steps before the drug can be given IV. These steps take time. The provider team must assure that the time needed to prepare and administer the amiodarone does NOT delay the fourth or even the fifth shock or subsequent epinephrine doses.4
Dosage: In VF/pulseless VT, 300 mg of amiodarone is administered as a rapid IV bolus. If pre-filled amiodarone syringe is not available, dilute with saline or D5W to a total volume of 20 to 30 mL. Supplementary doses of 150 mg by rapid IV infusion may be administered for refractory or recurrent VF/VT. In successful resuscitations with amiodarone, follow the above bolus doses with an infusion of 1 mg/min for 6 hours and then 0.5 mg/min up to a maximum cumulative dose of 2.2 g over 24 hours.2 PEDS: 5 mg/kg IV/IO initial dose; repeat as needed to maximum of 15 mg/kg
D. Magnesium sulfate (Class IIb recommendation)
Magnesium has demonstrated effectiveness in two clinical situations: the treatment of torsades de pointes, for which it has a Class IIa recommendation and VT/VF and other arrhythmias associated with known hypomagnesemia (Class IIb).4
Dosage: In cardiac arrest (for hypomagnesemia or torsades de pointes), give 1 to 2 g of magnesium sulfate diluted in 10 mL of D5W IV push. In torsades de pointes (not cardiac arrest), give a loading dose of 1 to 2 g mixed in 50 to 100 mL of D5W over 5 to 60 minutes IV, followed with 0.5 to 1.0 g/h IV for up to 24 hours. Since rapid administration of magnesium sulfate can cause severe hypotension or asystole, the very rapid infusion of magnesium sulfate as described here should be avoided except in the most urgent situations.2
E. Sodium bicarbonate
Individualize the use of sodium bicarbonate in cardiac arrest to the clinical setting. When indicated, a dose of 1 mEq/kg IV/IO may be appropriate.
Sodium Bicarbonate Recommendations
Class I - For patients known to be hyperkalemic
Other situations in which buffer therapy may be considered:
-
For patients with known or suspected preexisting bicarbonate—responsive acidosis and metabolic acidosis due to bicarbonate losses (GI or renal)
-
To alkalize the serum in severe tricyclic overdose
-
To alkalize the urine in certain drug overdoses, such as phenobarbital or aspirin
-
For patients who are intubated and have been in protracted cardiac arrest
-
For patients in protracted cardiac arrest who experience return of spontaneous circulation
Sodium bicarbonate is not indicated for patients with hypoxic lactic acidosis.
F. Special Drug Needs in Ventricular Fibrillation/Ventricular Tachycardia
Especially in persistent/recurrent VF/VT, the resuscitation team must consider potential treatable causes for the VF/FT:
-
Hyperkalemia (K+ > 6 mEq/L) needs treatment with calcium chloride 8 to 16 mg/kg (5 to 10 cc of the 10% prefill solution) IV bolus followed by insulin, glucose, and bicarbonate.
-
Hypokalemia (often present with hypomagnesemia) needs treatment with potassium chloride 10 mEq IV diluted in 100 cc NS or D5W over 30 minutes.
-
Hypomagnesemia needs treatment with magnesium sulfate 1 to 2 grams IV.
-
If sinus bradycardia precedes the fibrillation, consider use of atropine IV and/or transcutaneous pacing.
-
If rapid tachycardia precedes the fibrillation, excess epinephrine or endogenous catecholamines may be present. Do not give additional doses of epinephrine IV; administer a beta blocker (such as metoprolol 5 mg IV).
Special Considerations: For patients with an implanted pacemaker or automatic cardioverter-defibrillator, rescuers must be careful not to place the external defibrillator paddle or pads over the generator unit. (A part of the defibrillation current may block or damage the implanted device.) For patients with an implanted defibrillator who are in VF: proceed with external defibrillation per protocol if the patient's own defibrillator does not discharge within 20 to 30 seconds. A rescuer touching a patient with an automatic implanted defibrillator when it discharges may feel a mild shock, but chance of injury to the rescuer is unlikely.
For a hypothermic patient with VF/VT who does not convert after the first 3 shocks, proper treatment requires re-warming the patient in addition to general resuscitation efforts. No further shocks should be administered until the patient's core temperature is > 30°C (86°F) and the patient’s rhythm has not spontaneously converted during the rewarming period.
Do not place the defibrillator paddle or pads over a nitroglycerin patch. The patch may cause arcing of the electric current, burn the patient, or decrease defibrillator current transmission.
Post-Resuscitation Care: Therapeutic Hypothermia
A number of clinical trials and systematic reviews4,5 suggest that intentionally induced hypothermia after successful resuscitation from some types of cardiac arrest improves both survival and neurological recovery. Due to inconsistent methodology, it has been difficult to generalize these findings to all cases of cardiac arrest.
In 2005, the International Liaison Commission on Resuscitation (ILCOR) made the following recommendation6:
“Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32°C to 34°C [89°F to 93°F] for 12 to 24 hours when the initial rhythm is VF. Cooling to 32°C to 34°C for 12 to 24 hours may be considered for unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest from any other rhythm or cardiac arrest in hospital.”
Due to lack of evidence, there is no similar recommendation for pediatric patients or for other types of cardiac arrest (asystole, PEA); however, application of this therapy in these settings may be a reasonable option.
Methods of inducing hypothermia include application of ice packs to neck, axillae and groin as well as use of cooling blankets and jackets (eg, Arctic Sun®). Administration of IV iced saline (up to 30 mL/kg of saline at 4°C [39.2°F]) has been also used,7 but beware of volume overload. Remember that hypothermic patients are susceptible to clotting abnormalities and bleeding.
References
- ECC Subcommittee, Subcommittees and Task Forces of the American Heart Association. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3):S735-S746.
- ECC Committee, ECC Subcommittees, and ECC Task Forces; and Authors of Final Evidence Evaluation Worksheets. 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care With Treatment Recommendations Conference. Circulation. 2005;112(24 suppl):b2-b5.
- Hazinski MF, Field JM, Gilmore D, editors. Handbook of Emergency Cardiovascular Care. Dallas, Tx: American Heart Association, 2008.
- Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557-563.
- Cheung KW, Green RS, Magee KD. Systematic review of randomized controlled trials of therapeutic hypothermia as a neuroprotectant in post cardiac arrest patients. CJEM. 2006;8:329-337.
- International Liaison Committee on Resuscitation. 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science and Treatment Recommendations. Part 4: Advanced life support. Resuscitation. 2005;67:213-247.
- Bernard S, Buist M, Monteiro O, Smith K. Induced hypothermia using large volume, ice-cold intravenous fluid in comatose survivors of out-of-hospital cardiac arrest: a preliminary report. Resuscitation. 2003;56:9-13.