eMedicine Specialties > Emergency Medicine > Cardiovascular
Ventricular Fibrillation: Treatment & Medication
Updated: Jul 28, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
Because of the critical importance of early defibrillation, prehospital care is vital for arrests due to 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.
- Traditionally, CPR consists of artificial respirations and chest compressions. Mounting evidence demonstrates that chest compressions are the critical action to provide some cardiac perfusion during CPR, and artificial respirations are less important. 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. Current guidelines recommend both artificial respirations and chest compressions for all patients as described in the algorithm below. Future guidelines may reflect developments in this ongoing area of research.
- 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.
- AEDs are programmed to recognize 3 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 3 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).
- Early access to trained EMS personnel capable of performing CPR, defibrillation, and advanced cardiac life support (ACLS)
Emergency Department Care
- Defibrillation
- Electrical external defibrillation remains the most successful treatment of 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.
- Successful defibrillation largely depends on the following 2 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 has a number of advantages over monophasic defibrillation including increased likelihood of defibrillation success for a given shocking energy. 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.
- Operators are advised to use the energy protocols associated with individual devices or to begin with 200 J.
- 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.
- 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.
- 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 algorithm below.
- 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 benefit of this intervention has been demonstrated in a prospective clinical trial, and it has now been included as an optional protocol for Emergency Medical Services (EMS) in the ACLS guidelines.{Ref1}
- 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.
- 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 also has converted VT to VF and VF to asystole in other cases. This intervention is no longer routinely recommended.
- Algorithm
- 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.
- Adult - Device specific or 200 J for biphasic waveform and 360 J for monophasic waveform
- 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.
- Five 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 the following are performed:
- Secure intravenous access.
- Perform endotracheal intubation.
- Once 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 the following:
- Rhythm check
- Defibrillation
- 2 minutes of CPR
- Vasopressors
- 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.
- 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 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.
- 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 angioplasty, and intra-aortic balloon pump placement.
- 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).
Consultations
Consult a cardiologist or intensivist for continued inpatient ICU care.
Medication
Treatment goals are to electrically terminate 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. Recent data suggest no synergistic effect of administering vasopressin in addition to epinephrine.
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.
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.
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. Propanolol 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.
Vasopressors/sympathomimetics
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.
Adult
1 mg (10 mL of 1:10,000 solution) IV push (IVP) or intraosseous (IO) q3-5min or 0.1 mg/kg IVP q3-5 min; intermediate doses of 2-5 mg IVP q3-5 min also may be used; dose may be increased, as follows: 1 mg, 3 mg, 5 mg IVP given at 3-min intervals; higher doses do not improve survival or neurologic outcome; ET administration requires 2-2.5 times the IV dose
Pediatric
0.01 mg/kg (0.1 mL/kg 1:10,000 solution) IVP or IO q3-5 min; 0.1 mg/kg (0.1 mL/kg 1:1,000 solution) recommended for ET administration
Increases toxicity of beta- and alpha-blocking agents and halogenated inhalational anesthetics
Documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma; local anesthesia in such areas such fingers or toes because vasoconstriction may produce sloughing of tissue; do not use during labor (may delay second stage of labor)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in elderly patients, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias
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.
Adult
40 U IV once only
Pediatric
Not recommended
Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects
Documented hypersensitivity; coronary artery disease
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia
Antidysrhythmics
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.
Adult
Bolus of 1-1.5 mg/kg IV; repeat prn using 1.5 mg/kg boluses q3-5 min, not to exceed 3 mg/kg; follow with continuous IV infusion of 2 mg/min after return of perfusion; if continuous IV infusion is not started, administer additional boluses of 0.5 mg/kg q10min to maintain effect
ET: Administer 2-2.5 times IV dose
Pediatric
ET, intraosseous (IO), and IV loading: 1 mg/kg (repeat dose twice at 10- to 15-min intervals prn)
Following loading dose, start continuous IV infusion of 20-50 mcg/kg/min
Coadministration with cimetidine or beta-blockers increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine
Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes syndrome and Wolff-Parkinson-White syndrome; avoid in severe sinoatrial, AV, or intraventricular block if artificial pacemaker is not in place
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Use a solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia, shock, respiratory-depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in elderly patients; high plasma concentrations can cause seizures, asystole, heart block, and AV conduction abnormalities
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.
Adult
300 mg IV bolus; 150 mg IV infused over 10 min, then 1 mg/min continuous infusion for 6 h; maintenance infusion at 0.5 mg/min
Pediatric
5 mg/kg IV or IO; repeat up to total 15 mg/kg, not to exceed 300 mg
Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels
Documented hypersensitivity; complete AV block; intraventricular conduction defects; patients taking ritonavir or sparfloxacin
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in thyroid or liver disease; hypotension (most common adverse effect), bradycardia, AV block, and torsades de pointes may occur; elevated serum hepatic enzyme levels are common in VT
Bretylium tosylate
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.
Adult
Initial dose: 5 mg/kg (undiluted) IV over 1 min; for persistent arrhythmia, 10 mg/kg (undiluted) IV over 1 min; repeat at 15-30 min intervals prn; not to exceed 30-35 mg/kg/24 h
Maintenance dose: 1-2 mg/min IV
Pediatric
Not established; suggested dose is 5 mg/kg IV over 1 min; if arrhythmia persists, 10 mg/kg IV over 1 min q15min prn; not to exceed 30 mg/kg; maintenance dose is 5-10 mg/kg/dose IV q6h
Increased toxicity reported when taken with pressor catecholamines and digitalis; may increase risk of cardiotoxicity when taken concurrently with sparfloxacin or ofloxacin
Documented hypersensitivity; systemic lupus erythematosus, digitalis-induced arrhythmias, complete heart block, or second- or third-degree heart block if a pacemaker is not in place; avoid in torsade de pointes
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause hypotension, especially in patients with fixed cardiac output (eg, aortic stenosis); caution in renal insufficiency, severe pulmonary hypertension, and aortic stenosis; half-life increases in elderly patients; with renal clearance of 10-50 mL/min, administer 25-50% of dose; rapid IV injections may result in transient hypertension, nausea, and vomiting; limit injection to 5 mL (undiluted) at each injection site
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.
Adult
25 mg/min IV at continued infusion rates until dysrhythmia is suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or a maximum dose of 17 mg/kg is administered; once arrhythmia is suppressed, may infuse at a continuous rate of 1-4 mg/min
Pediatric
Not established; the following doses have been suggested: 15-50 mg/kg/d PO divided q3-6h; not to exceed 4 g/d
20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d
3-6 mg/kg/dose IV infused over 5 min
Maintenance: 20-80 mcg/kg/min IV administered as continuous infusion; not to exceed 100 mg/dose or 2 g/d
Can expect increased levels of procainamide metabolite, NAPA, in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; procainamide may increase effect of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity
Documented hypersensitivity; complete heart block or second- or third-degree heart block if pacemaker is not in place; torsade de pointes; systemic lupus erythematosus
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Long-term use of this drug leads to development of positive antinuclear antibody test result in 50% of patients; may result in lupus erythematosus–like syndrome in about 20-30% of patients; fatal blood dyscrasias also have been reported with therapeutic doses; plasma concentration of procainamide and its active metabolite, NAPA, may be increased in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency
Electrolytes
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.
Adult
1-2 g diluted in 100 mL of D5W administered IV over period of 1-2 min for refractory VF and known or suspected hypomagnesemia (Mg+2 <1.4 mEq/L); not to exceed 30-40 g/d or 1-2 g/h maintenance rate
Pediatric
Not established; suggested dose is 25-50 mg/kg IV q4-6h for 3-4 doses; maximum single dose of 2 g may be administered and repeated if hypomagnesemia persists
Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and other agents causing neuromuscular antagonism; increases toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine
Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
May alter cardiac conduction leading to heart block in digitalized patients; when electrolytes are administered parenterally, monitor respiratory rate, deep tendon reflex, and renal function; may produce significant hypertension or asystole
Sodium bicarbonate (Neut)
Only when the patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, tricyclic antidepressant, or phenobarbital overdose. Routine use not recommended.
Adult
1 mEq/kg/dose IV initially followed by 0.5 mEq/kg/dose IV q10min or as indicated by ABGs
Pediatric
0.5-1 mEq/kg/dose IV repeated q10min or as indicated by ABGs; rate of infusion not to exceed 10 mEq/min
Urinary alkalinization, induced by increased sodium bicarbonate concentrations, may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine
Patients with alkalosis, hypernatremia, hypocalcemia, severe pulmonary edema, and unknown abdominal pain
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Only to be used to treat documented metabolic acidosis and hyperkalemia-induced cardiac arrest; can cause alkalosis, decreased plasma potassium level, hypocalcemia, and hypernatremia; caution in electrolyte imbalances, eg, patients with CHF, cirrhosis, edema, corticosteroid use, or renal failure; when administering, avoid extravasation since can cause tissue necrosis
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.
Adult
Known or suspected hyperkalemia (K+ > 6 mEq/L): 2-4 mg/kg (10% solution) IV
Pediatric
0.2 mL/kg of IV (10% solution)
Coadministration with digoxin may cause arrhythmias; with thiazides, may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate
VF not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure
More on Ventricular Fibrillation |
| Overview: Ventricular Fibrillation |
| Differential Diagnoses & Workup: Ventricular Fibrillation |
 Treatment & Medication: Ventricular Fibrillation |
| Follow-up: Ventricular Fibrillation |
| Multimedia: Ventricular Fibrillation |
| References |
| « Previous Page | Next Page » |
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Further Reading
Keywords
VF, ventricular fibrillation, sudden cardiac death, SCD, tachycardia, ventricular tachycardia, VT, pulseless electrical activity, PEA, asystole, acute cardiac ischemia, acute cardiac infarction, acute myocardial infarction, MI, cardiac arrest
