Download Ventricular Fibrillation (2)

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Florida Heart CPR*
Ventricular Fibrillation
Objectives:
After reading the information the student will be able to:
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Assess and define ventricular fibrillation
Demonstrate competency in managing ventricular fibrillation
Identify anti-arrhythmic medications and dosages
Understand the conduction system of the heart
Ventricular Fibrillation (VF) is the single most important rhythm for nurses and medical
professionals to recognize. It is a rhythm in which multiple areas within the ventricles display
marked variation in depolarization and repolarization. Since there is no organized ventricular
depolarization, the ventricles do not contract as a unit. When observed directly, the ventricular
myocardium appears to be quivering. There is no cardiac output. This is the most common
mechanism of cardiac arrest resulting from myocardial ischemia or infarction. The terms coarse
and fine have been used to describe the amplitude of the waveforms in VF. Coarse VF usually
indicates the recent onset of VF, which can be readily corrected by prompt defibrillation. The
presence of fine VF that approaches asystole often means there has been a considerable delay
since collapse, and successful resuscitation is more difficult.
Initial treatment is always defibrillation. Only defibrillation provides definitive therapy. The
exact benefit of anti-fibrillatory agents on persistent VF independent of defibrillation is
unknown. Because their contribution (if any) remains doubtful, never delay defibrillation while
waiting for pharmacologic agents to have an effect.
Introduction
In order to understand what is occurring during ventricular fibrillation, it is important to have a
working knowledge of some cardiac anatomy and physiology.
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Heart Chambers
The heart is a four chambered structure made up of two receiving chambers called atria and two
pumping chambers called ventricles. The right atrium receives oxygen poor blood returning
from the body through the superior and inferior vena cava. The right ventricle pushes the oxygen
poor blood to the lungs through the pulmonary arteries. The left atrium receives oxygen rich
blood returning from the lungs through pulmonary veins. The left ventricle pushes the oxygen
rich blood out through the aorta, which directs the blood to all parts of the body. The right and
left atria are separated by the interatrial septum while the right and left ventricles are separated
by the interventricular septum.
Heart Valves
When blood flows through the heart it follows a unidirectional pattern. It first enters both atria
and then fills both ventricles before leaving the heart. In order to prevent backflow against this
pattern there are four valves in the heart that serve this function.
Found between the atria and ventricles are two atrioventricular (A-V) valves that prevent blood
from reentering the atria. The valve that guards the right atrium is called the tricuspid valve
while the valve guarding the left atrium is called the bicuspid or mitral valve.
The two remaining valves are called semi lunar valves. The valve located where the pulmonary
trunk meets the right ventricle is called the pulmonary semi lunar valve. The valve found
where the aorta and left ventricle meet is called the aortic semi lunar valve. Both semi lunar
valves prevent backflow of blood into the ventricles.
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Heart Muscle (Myocardium)
The heart is a specialized structure, which is made of muscle that has unique characteristics. The
cell membranes of myocardial cells form very close connections to each other. These
connections are called intercalated disks and allow groups of muscle cells to function as one.
This unique contractile ability of myocardium is known as a syncytium. The muscle cells that
make up the atria and ventricles act as two separate syncytia, therefore contracting as two single
units.
Cardiac muscle has the ability to adapt to the amount of blood being delivered to it. There is a
direct proportion between the amount of blood returning to the heart and the force of cardiac
muscle contraction. The more blood returning through the veins, the stronger the muscular
contraction ejecting blood out of the heart into the arteries. This occurs due to the heart
muscle responding to a stretch in the chamber walls as a result of an increased amount of blood
volume entering the heart. The ability of the heart to be able to equalize the amount of blood
entering and exiting it is called Frank-Starling’s law of the heart.
Compared to skeletal muscle, heart muscle cells have a longer rest or refractory period. This
allows the myocardium to relax after each contraction preventing a tetanic contraction of the
heart. It also gives the heart chambers time to fill with blood before the next contraction.
Unlike skeletal muscle, which needs nerve innervation for stimulation, cardiac muscle needs no
outside stimulus. This is what is known as automaticity. Heart muscle also possesses inherent
rhythm, which means it will contract at a regular rate.
Conduction System
The conduction system of the heart explains how heart muscle has automaticity and is able to
contract without the help of outside nervous or hormonal innervation. It is made up of
specialized cardiac cells that initiate and guide myocardial contraction. The conduction system
consists of the sinoatrial node (S-A node), atrioventricular node (A-V node), atrioventricular
bundle (A-V bundle or A-V bundle of His), Purkinje fibers and bundle branches.
The S-A node is located in the posterior wall of the right atrium. It sets off impulses that trigger
atrial contraction. It discharges impulses quicker than any other part of the heart and establishes
the rate and rhythm for the entire heart. Because of this it is more commonly known as the
pacemaker.
The contracted atrial cells then send the impulse to the A-V node, which is located in the atrial
wall near the interatrial septum. Once the A-V node picks up the signal, the speed of impulse
transmission is slowed down to allow the atria time to complete contraction before ventricular
contraction occurs.
From the A-V node the impulse then travels to the A-V bundle (bundle of His) which is made
up of special fibers called Purkinje fibers. The A-V bundle begins at the right side of the
interatrial septum and runs down to the beginning of the interventricular septum. It then branches
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into right and left bundle branches that run down the length of the interventricular septum. The
bundle branches further divide into Purkinje fibers that cover the inner surface of the ventricles.
The impulses relayed from the Purkinje fibers initiates ventricular contraction.
Definition of Ventricular Fibrillation
Ventricular fibrillation is defined as a cardiac arrhythmia identified by rapid, disorganized
depolarization's of ventricular heart muscle. It is characterized by a complete lack of organized
electric impulse, conduction and ventricular contraction. This leads to the incapability of the
ventricles to pump sufficient blood (if any) out of the heart to the entire body. Blood pressure
and circulation become compromised as a result. Ventricular fibrillation is the most common
rhythm present following onset of cardiac arrest in adults.
Identification of
Ventricular Fibrillation/Ventricular Tachycardia
Before one can manage a patient in ventricular fibrillation, it is important to correctly identify
said condition. The following rhythm strips are examples of ventricular fibrillation/ventricular
tachycardia.
Fig 2 Coarse VF
Coarse VF usually indicates the recent onset of VF, which can be readily
corrected by prompt defibrillation.
Fig 3 Fine VF
The presence of fine VF that approaches asystole often means there has been
a considerable delay since collapse, and successful resuscitation is more
difficult.
Fig 4 Ventricular Tachycardia (VT)
Pulseless VT should be treated identically as VF
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Management of Ventricular Fibrillation
There is a specific protocol or algorithm one must follow once ventricular fibrillation is
confirmed.
The American Heart Association suggests the following guidelines.
1. Once ventricular fibrillation is determined, call for a defibrillator. While waiting for
defibrillator to be attached, perform CAB (Circulation, Airway, Breathing,, ). *Note: CPR
must be performed until defibrillator has arrived.
The Purpose of Defibrillation
Defibrillation does not "jump start" the heart. The purpose of the shock is to produce temporary
asystole. The shock attempts to completely depolarize the myocardium and provide an
opportunity for the natural pacemaker centers of the heart to resume normal activity. During
asystole cardiac rhythmicity will resume if sufficient stores of high-energy phosphates remain in
the myocardium. The fibrillating myocardium consumes these stores at a greater rate than
normal cardiac rhythms do. Thus, early defibrillation, before fibrillation consumes all these
energy stores, becomes critical.
What about a Precordial Thump
The precordial thump is acceptable and possibly helpful when witnessed arrest, no pulse, and no
defibrillator is immediately available. A forceful precordial thump can convert patients out of VFib and into a perfusing cardiac function.
Caution: This thump can also convert patients from coordinated cardiac activity into VFib or asystole.
Note: If a defibrillator is available, go directly to that therapy and not waste even a minimum
of time with the precordial thump.
2. Once a defibrillator arrives, defibrillate as soon as possible. The first shock should be set
at the manufacturer's recommended dose to terminate V-Fib on the first shock (1st shock
efficacy). This may be 120-150 joules. Subsequent shocks can be increased in a stepwise
fashion, however in most current monitor defibrillators that are biphasic, 200 joules may
be the highest dose.
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No Pulse Checks Between Shocks
The nurse or medical professional should resume CPR while he/she recharges the defibrillator.
At this point in the treatment sequence, do not pause for a pulse check if a properly connected
monitor clearly displays persistent VF/VT. Look immediately at the monitor screen (while
recharging) to check for persistent VF/VT. If a non–VF/VT rhythm appears on the monitor,
check a carotid pulse.
Nitroglycerin Patches
If the patient has placed a nitroglycerin patch on his or her chest, remove it or make sure the
defibrillation electrode does not touch the patch. Despite concern about potential volatility, the
nitroglycerin substrate will not burn or "explode." However, the aluminized backing used on
some old transdermal delivery systems can lead to electrical arcing during defibrillation, with
explosive noises, smoke, visible arcing, and patient burns. The patches may also impair the
transmission of current. Most aluminized backing systems have been discontinued.
Implanted Pacemakers/Cardioverters-Defibrillators
Nurses should avoid placing defibrillator pads over an implanted pacemaker or automatic
cardioverter-defibrillator. Defibrillation directly over an implanted pacemaker or
automatic cardioverter-defibrillator may block a part of the defibrillation current and possibly
misprogram, disable, or severely damage the implanted device. Discharges from automatic
implanted defibrillators can be felt by rescuers if they touch the patient during the shock, though
the chances of harm to the rescuer are extremely remote.
Witnesses may report that the implanted defibrillator has discharged or is in the midst of a
charge-discharge cycle. Rescuers should monitor patients with implanted defibrillators and
observe if the patient is in VF or refibrillates. Most implantable defibrillators will assess charge
and shock within 20 to 30 seconds. If the patient appears in VF and the implanted defibrillator is
not delivering a shock, proceed with defibrillation protocols.
4. If persistent or recurring ventricular fibrillation:
A. Continue CPR
B. Maintain a patent airway
C. Obtain IV access
*Note: All drugs that are administered should be alternated with defibrillation.
(i.e.) Shock; drug, shock, drug etc.
5. Administer epinephrine. Remember we give Epi, at least 1mg Q 3-5 min. for every code.
The recommended dose of epinephrine is 1 mg IV push every 3 to 5 minutes. If this approach
fails, several other dosing regimens can be considered:
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Epinephrine, at the standard dose of 1 mg given IV every 3 to 5 minutes, remains the drug of
choice for patients in cardiac arrest. Clinicians and researchers have conducted extensive
research on the use of adrenergic medications in cardiac arrest. No agent has proven superior to
epinephrine for increasing blood flow and improving outcomes. Clinicians should place a high
priority on early administration of this agent. Epinephrine stimulates adrenergic receptors and
produces increased blood flow to the brain and heart.
At the next rhythm check, and after the first dose of epinephrine, the nurse should reassess the
rhythm and if VF/VT is present deliver an additional shock.
6. To ensure safe defibrillation, people who perform defibrillation must always announce when
they are about to shock. The person who controls the defibrillator should state, firmly and in a
forceful voice, a "warning chant" before each shock. The operator should check and make sure
he or she has no contact with the patient, the stretcher, or other equipment. The operator should
then check the personnel doing ventilations and chest compressions, who should remove their
hands from the ventilatory adjuncts, including the endotracheal tube and ventilation bags. The
operator should also make a visual check to ensure that no one else has contact with the patient
or stretcher. The operator must warn others that he or she is about to defibrillate and that
everyone needs to stand clear.
7. Administer antiarrhythmic medication in persistent or recurring ventricular fibrillation.
Amiodarone
If VF/VT persists after CPR, ventilation, shock, and one dose of epinephrine, rescuers are
dealing with refractory or persistent VF. In addition, minutes have passed during which the
patient has likely received only modest blood flow (10% to 30% of normal) from conventional
closed-chest CPR.
The chances now of the patient's regaining spontaneous circulation and a successful neurological
outcome are low. Typically at this point in the protocol, rescuers administer an antifibrillatory
agent, such as Amiodarone. They should follow this with a shock. Rescuers must understand that
it is not the pharmacologic agent that defibrillates the heart but the direct current shock.
The dosage of amiodarone in refractory VF/VT is 300mg IV push. The second dose (after
another shock and another Epi) is 150mg IV push. Drugs administered during cardiac arrest
should preferably be given while CPR is in progress, in order to circulate the drug most
effectively. If Amiodarone is unavailable, Lidocaine can be used. First dose is 1-1.5mg/kg and
second scheduled dose is .05-.75mg/kg.
Electricity vs Antiarhythmics
The spread of early defibrillation programs represents a natural experiment about the relative
effectiveness of early defibrillation alone versus defibrillation plus late medication. It is difficult
in human clinical studies to confirm an independent positive benefit from IV medications.
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Refractory or Recurrent Ventricular Fibrillation
Magnesium sulfate is another medication to consider in VF/VT that persists after
multiple shocks, epinephrine, and while considering history of arrhythmias or torsades de
pointes.
IV. Magnesium sulfate
Administer magnesium sulfate 1 to 2 g IV push in patients with known or suspected
hypomagnesemia (eg, patients with alcoholism or other conditions associated with
malnutrition). Use magnesium at the same dose or higher for patients with a torsades de pointes
pattern of VF or VT. The success of magnesium sulfate in prevention of VF/VT in the setting of
acute MI patients has generated great hope for magnesium sulfate as an anti-arrhythmic to use in
cardiac arrest due to refractory VF/VT. In large doses, magnesium sulfate lowers the blood
pressure, but this may not necessarily compromise coronary perfusion pressure because it also
dilates coronary arteries. The value of magnesium in human cardiac arrest has not been
demonstrated in randomized controlled trials, though encouraging anecdotal successes have
been reported.
*Note: Magnesium Sulfate should be administered 1-2 g IV in torsades de pointes or suspected
hypomagnesemic state.
Fig. 5 Torsades de pointes
The Value of Interposed Non–VF Rhythms During VF Treatment
Faced with persistent, refractory, or recurrent VF, astute clinicians will not continue with cycles
of electric shocks and escalating drug doses. They should think in terms of the basics of
resuscitation: adequate CPR, adequate airway and ventilation, and properly administered
pharmacologic agents. Clinicians should consider coexisting electrolyte abnormalities and
medication side effects. The non–VF cardiac rhythms that immediately follow shocks or that
precede refibrillation may offer a clue to causes and interventions.
For example, epinephrine or excessive levels of endogenous catecholamines may be playing a
role if a rapid tachycardia precedes the refibrillation. In these situations the team leader should
consider withholding further doses of epinephrine, particularly if doses higher than 1 mg were
used, and giving ß blockers, such as metoprolol 5 mg IV. If a sinus or AV bradycardia precedes
the refibrillation, the clinician should consider the addition of fluids, pressors, or the use of
transcutaneous pacing (TCP). Electrolyte abnormalities, particularly potassium and magnesium,
may produce immediate post shock refibrillation or persistent VF.
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Known or suspected hyperkalemia (serum potassium level higher than 6 mmol/L [6 mEq/L])
should be treated with calcium chloride 4 mg/kg acutely followed by insulin, glucose, and
sodium bicarbonate. Hypokalemia is often associated with low magnesium (less than 0.7
mmol/L [1.4mEq/L]) and should be treated with potassium chloride 10 mEq IV slowly over 10
to 15 minutes using a diluted solution.
V. Sodium Bicarbonate
Sodium bicarbonate has a variable status. Some researchers and clinicians have conducted the
"bicarbonate debate" in absolute terms. Emergency personnel either give bicarbonate in cardiac
arrest or completely avoid it. As with most areas in clinical medicine, however, bicarbonate
therapy requires clinical judgment and modifications based on each clinical situation. In this
regard there appropriate indication exists.
Sodium bicarbonate (1 mEq/kg) if the patient is known to be hyperkalemic.
For patients with known or suspected preexisting bicarbonate-responsive acidosis and
metabolic acidosis due to bicarbonate losses (gastrointestinal or renal)
To alkalinize the serum in severe tricyclic overdose.
To alkalinize the urine in certain drug overdoses, such as phenobarbital or aspirin (this,
of course, is an impractical therapeutic goal during cardiac arrest and applies in
general to such overdoses).
For patients who are intubated and have been in protracted cardiac arrest .
For patients with protracted cardiac arrest who experience return of spontaneous
circulation.
Sodium bicarbonate is not indicated and is possibly harmful in patients with hypoxic lactic
acidosis, such as occurs in prolonged cardiopulmonary arrest. In such clinical situations the
accumulation of metabolic byproducts, not bicarbonate deficits, has produced the acidosis. No
evidence demonstrates that buffering the arterial pH with bicarbonate in such
circumstances benefits the patient, and some evidence suggests it is harmful.
Maintenance Antiarrhythmics After Return of Spontaneous Circulation
Once VF/VT has resolved after the sequence of treatment outlined above, clinicians should begin
an IV infusion of the antiarrhythmic that appeared to aid in the restoration of a pulse. If
defibrillation alone led to a restored circulation, the patient should be given a pharmacologic
loading dose of amiodarone, starting with 150mg mixed in a 50cc or 100cc bag of saline or D5,
and bolused over 10 minutes (15mg/min).
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Upon Return Of Spontaneous Circulation (ROSC).....
B/P, 12 Lead, therapeutic hypothermia protocol......while:
- Assessing vital signs
- Maintain or upgrading airway
-Provide medications appropriate for blood pressure, heart rate and rhythm
References: 2010 and 2015 American Heart Association, and International Liaison
Committee on Resuscitation (ILCOR).
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Ventricular Fibrillation Assessment
1. This is a rhythm in which multiple areas within the ventricles display marked variation in
depolarization and repolarization.
a. Atrial fibrillation
b. Ventricular fibrillation
c. Sinus tachycardia
d. Sinus bradycardia
2. _______ usually indicates the recent onset of VF, which can be readily corrected by
prompt defibrillation.
a. Fine VF
b. Coarse VF
c. Recurrent VF
d. Recent VF
3. Unlike skeletal muscle, which needs nerve innervation for stimulation, cardiac muscle
needs no outside stimulus. This is what is known as
a. Inherent innervation
b. Cardiac rhythm
c. Autonomic rhythm
d. Automaticity
4. The _____ is located in the posterior wall of the right atrium. It sets off impulses that
trigger atrial contraction. It discharges impulses quicker than any other part of the heart
and establishes the rate and rhythm for the entire heart. Because of this it is more
commonly known as the pacemaker.
a. S-A node
b. A-V node
c. Bundle of His
d. Purkinje fibers
5. ________ is defined as a cardiac arrhythmia identified by rapid, disorganized
depolarization's of ventricular heart muscle. It is characterized by a complete lack of
organized electric impulse, conduction and ventricular contraction.
a. Atrial fibrillation
b. Ventricular fibrillation
c. Ventricular tachycardia
d. Ventricular disorganization
6. The _______ is acceptable and possibly helpful when witnessed arrest, no pulse, and no
defibrillator is immediately available. A forceful _______ can convert patients out of VFib and into a perfusing cardiac function.
a. Precordial shock
b. Precordial defibrillation
c. Atrial defibrillation
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d. Precordial thump
7. _______, at the standard dose of 1 mg given IV every 3 to 5 minutes, remains the drug of
choice for patients in cardiac arrest.
a. Norepinephrine
b. Epinephrine
c. Acetosalicylic acid
d. Morphine
8. If VF/VT persists after basic CPR, ventilation, defibrillation, and one dose of
epinephrine, rescuers are dealing with refractory or persistent VF. Typically at this point
in the protocol, rescuers administer an antifibrillatory agent, such as:
a. Lidocaine
b. Amiodarone
c. Procainamide
d. Any of the above
9. _______ is another medication to consider in VF/VT that persists after multiple shocks,
epinephrine, and amiodarone.
a. Procainamide
b. Magnesium sulfate
c. Both A and B
d. Neither A nor B
10. _______ has a variable status. Emergency personnel either give it in cardiac arrest or
completely avoid it. It is given to treat acidosis.
a. Magnesium sulfate
b. Magnesium bicarbonate
c. Sodium bicarbonate
d. Any of the above
Florida Heart CPR* 2015 guidelines