Ventricular fibrillation

Ventricular fibrillation (V-fib or VF) is a condition in which there is uncoordinated

contraction of the cardiac muscle of the ventricles in the heart, making them quiver
rather than contract properly. Ventricular fibrillation is the most commonly identified
arrhythmia in cardiac arrest patients. While there is some activity, the lay person is
usually unable to detect it by palpating (feeling) the major pulse points of the carotid
and femoral arteries. Such an arrhythmia is only confirmed by electrocardiography.
Ventricular fibrillation is a medical emergency that requires prompt Advanced Life
Support interventions. If this arrhythmia continues for more than a few seconds, it will
likely degenerate further into asystole ("flatline"). This condition results in cardiogenic
shock and cessation of effective blood circulation. As a consequence, sudden cardiac
death (SCD) will result in a matter of minutes. If the patient is not revived after a
sufficient period (within roughly 5 minutes at room temperature), the patient could
sustain irreversible brain damage and possibly become brain-dead, due to the effects of
cerebral hypoxia. On the other hand, death often occurs if sinus rhythm is not restored
within 90 seconds of the onset of VF, especially if it has degenerated further into
asystole.
Contents
Signs and symptoms
Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The
ventricular muscle twitches randomly rather than contracting in a coordinated fashion
(from the apex of the heart to the outflow of the ventricles), and so the ventricles fail to
pump blood into the arteries and systemic circulation. Ventricular fibrillation is a sudden
lethal arrhythmia responsible for many deaths in the Western world, and it is mostly
caused by ischemic heart disease. While most episodes occur in diseased hearts, others
can afflict normal hearts as well.
Despite considerable research, the underlying nature of ventricular fibrillation is still not
completely understood.
Symptoms can include sudden collapse of the individual with no preceding signs of
distress. First hand accounts have described one instance
[citation needed]
where the victim
appeared to be having a seizure followed by a sudden color change from flushed red to
blue with no detectable pulse. In this instance CPR, compressions and resuscitation
breathing, was immediately started followed by 2 discharges from an AED (automated
external defibrillator) and two more discharges by trained EMTs. Complete patient
recovery was credited to the quick response.
First hand accounts of another instance where the victim had no symptoms and
collapsed followed by a sudden color change to blue with no detectable pulse. In this
instance as well, CPR was immediately started without the use of an AED. EMT workers
arrived within 5 minutes of the collapse, discharged an AED multiple times, but were
unable to gain normal cardiac rhythm. Continuous chest compressions and intubation for
45 minutes allowed transport of the patient to a hospital where an emergency team
were able to resuscitate the victim. The victim suffered no hypoxic damage. Subsequent
examination revealed no heart disease. Patient was implanted with a defibrillator.
Cause
Abnormal automaticity
Automaticity is a measure of the propensity of a fiber to initiate an impulse
spontaneously. The product of a hypoxic myocardium can be hyperirritable myocardial
cells. These may then act as pacemakers. The ventricles are then being stimulated by
more than one pacemaker. Scar and dying tissue is inexcitable, but around these areas
usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may
generate re-entry ventricular arrhythmia.
It is interesting to note that most cardiac myocardial cells with an associated increased
propensity to arrhythmia development have an associated loss of membrane potential.
That is, the maximum diastolic potential is less negative and therefore exists closer to
the threshold potential. Cellular depolarisation can be due to a raised external
concentration of potassium ions K
+
, a decreased intracellular concentration of sodium
ions Na
+
, increased permeability to Na
+
, or a decreased permeability to K
+
. The ionic
basic automaticity is the net gain of an intracellular positive charge during diastole in the
presence of a voltage-dependent channel activated by potentials negative to 50 to
60 mV.
Myocardial cells are exposed to different environments. Normal cells may be exposed to
hyperkalaemia; abnormal cells may be perfused by normal environment. For example,
with a healed myocardial infarction, abnormal cells can be exposed to an abnormal
environment such as with a myocardial infarction with myocardial ischaemia. In
conditions such as myocardial ischaemia, possible mechanism of arrhythmia generation
include the resulting decreased internal K
+
concentration, the increased external K
+

concentration, norepinephrine release and acidosis. When myocardial cell are exposed to
hyperkaliemia, the maximum diastolic potential is depolarized as a result of the
alteration of Ik1 potassium current, whose intensity and direction is strictly dependent
on intracellular and extracellular potassium concentrations. With Ik1 suppressed, an
hyperpolarizing effect is lost and therefore there can be activation of funny current even
in myocardial cells (which is normally suppressed by the hyperpolarizing effect of
coexisting potassium currents). This can lead to the instauration of automaticity in
ischemic tissue.
Re-entry
The role of re-entry or circus motion was demonstrated separately by Mines and
Garrey. Mines created a ring of excitable tissue by cutting the atria out of the ray fish.
Garrey cut out a similar ring from the turtle ventricle. They were both able to show that,
if a ring of excitable tissue was stimulated at a single point, the subsequent waves of
depolarisation would pass around the ring. The waves eventually meet and cancel each
other out, but, if an area of transient block occurred with a refractory period that
blocked one wavefront and subsequently allowed the other to proceed retrogradely over
the other path, then a self-sustaining circus movement phenomenon would result. For
this to happen, however, it is necessary that there be some form of non-uniformity. In
practice, this may be an area of ischaemic or infarcted myocardium, or underlying scar
tissue.
It is possible to think of the advancing wave of depolarisation as a dipole with a head
and a tail. The length of the refractory period and the time taken for the dipole to travel
a certain distancethe propagation velocitywill determine whether such a
circumstance will arise for re-entry to occur. Factors that promote re-entry would include
a slow-propagation velocity, a short refractory period with a sufficient size of ring of
conduction tissue. These would enable a dipole to reach an area that had been
refractory and is now able to be depolarised with continuation of the wavefront.
In clinical practice, therefore, factors that would lead to the right conditions to favour
such re-entry mechanisms include increased heart size through hypertrophy or
dilatation, drugs which alter the length of the refractory period and areas of cardiac
disease. Therefore, the substrate of ventricular fibrillation is transient or permanent
conduction block. Block due either to areas of damaged or refractory tissue leads to
areas of myocardium for initiation and perpetuation of fibrillation through the
phenomenon of re-entry.
Pathophysiology
Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity
of the heart" (Moe et al. 1964). A more complete definition is that ventricular fibrillation
is a "turbulent, disorganized electrical activity of the heart in such a way that the
recorded electrocardiographic deflections continuously change in shape, magnitude and
direction".Ventricular fibrillation most commonly occurs within diseased hearts, and, in
the vast majority of cases, is a manifestation of underlying ischemic heart disease.
Ventricular fibrillation is also seen in those with cardiomyopathy, myocarditis, and other
heart pathologies. In addition, it is seen with electrolyte disturbances and overdoses of
cardiotoxic drugs. It is also notable that ventricular fibrillation occurs where there is no
discernible heart pathology or other evident cause, the so-called idiopathic ventricular
fibrillation.
Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of
all cases of out-of-hospital arrest, as well as 3%-9% of the cases of ventricular
fibrillation unrelated to myocardial infarction, and 14% of all ventricular fibrillation
resuscitations in patients under the age of 40. It follows then that, on the basis of the
fact that ventricular fibrillation itself is common, idiopathic ventricular fibrillation
accounts for an appreciable mortality. Recently described syndromes such as the
Brugada Syndrome may give clues to the underlying mechanism of ventricular
arrhythmias. In the Brugada syndrome, changes may be found in the resting ECG with
evidence of right bundle branch block (RBBB) and ST elevation in the chest leads V1-V3,
with an underlying propensity to sudden cardiac death.
The relevance of this is that theories of the underlying pathophysiology and
electrophysiology must account for the occurrence of fibrillation in the apparent
"healthy" heart. It is evident that there are mechanisms at work that we do not fully
appreciate and understand. Investigators are exploring new techniques of detecting and
understanding the underlying mechanisms of sudden cardiac death in these patients
without pathological evidence of underlying heart disease.
Familial conditions that predispose individuals to developing ventricular fibrillation and
sudden cardiac death are often the result of gene mutations that affect cellular
transmembrane ion channels. For example, in Brugada Syndrome, sodium channels are
affected. In certain forms of long QT syndrome, the potassium inward rectifier channel
is affected.
Triggered activity
Triggered activity can occur due to the presence of afterdepolarisations. These are
depolarising oscillations in the membrane voltage induced by preceding action
potentials. These can occur before or after full repolarisation of the fiber and as such are
termed either early (EADs) or delayed afterdepolarisations (DADs). All
afterdepolarisations may not reach threshold potential, but, if they do, they can trigger
another afterdepolarisation, and thus self-perpetuate.
Characteristics of the ventricular fibrillation waveform
Ventricular fibrillation can be described in terms of its electrocardiographic waveform
appearance. All waveforms can be described in terms of certain features, such as
amplitude and frequency. Researchers have looked at the frequency of the ventricular
fibrillation waveform to see if it helps to elucidate the underlying mechanism of the
arrhythmia or holds any clinically useful information. More recently, Gray has suggested
an underlying mechanism for the frequency of the waveform that has puzzled
investigators as possibly being a manifestation of the Doppler effect of rotors of
fibrillation.
[8]
Analysis of the fibrillation waveform is performed using a mathematical
technique known as Fourier analysis.
Power spectrum


The distribution of frequency and power of a waveform can be expressed as a power
spectrum in which the contribution of different waveform frequencies to the waveform
under analysis is measured. This can be expressed as either the dominant or peak
frequency, i.e., the frequency with the greatest power or the median frequency, which
divides the spectrum in two halves.
Frequency analysis has many other uses in medicine and in cardiology, including
analysis of heart rate variability and assessment of cardiac function, as well as in
imaging and acoustics.
Histopathology

Myofibre break-up, abbreviated MFB, is associated with ventricular fibrillation leading to
death.
]
Histomorphologically, MFB is characterized by fractures of the cardiac myofibres
perpendicular to their long axis, with squaring of the myofibre nuclei.
Treatment
Defibrillation
Electric defibrillator
The condition can often be reversed by the electric discharge of direct current from a
defibrillator. Although a defibrillator is designed to correct the problem, and its effects
can be dramatic, it is not always successful.
Implantable electric defibrillator
In patients at high risk of ventricular fibrillation, the use of an implantable cardioverter
defibrillator has been shown to be beneficial.
Precordial thump
If no defibrillator is available, a precordial thump can be delivered at the onset of VF for
a small chance to regain cardiac function. A precordial thump may only be delivered if a
cardiac arrest is witnessed (someone sees the patient arrest) and if the arrest is
monitored (as seen on a cardiac monitor). However, research has shown that the
precordial thump releases no more than 30 joules of energy This is far less than the
200360 J typically used to bring about normal sinus rhythm.
Antiarrhythmic agents
Antiarrhythmic agents like amiodarone or lidocaine can help, but, unlike atrial fibrillation,
ventricular fibrillation rarely reverses spontaneously in large adult mammals. Drug
therapy with antiarrhythmic agents in ventricular fibrillation does not replace
defibrillation and is not the first priority, but is sometimes needed in cases where initial
defibrillation attempts are not successful.