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Articles
& Thesis
NEAR DEATH EXPERIENCES
IN CARDIAC ARREST:
VISIONS OF A DYING BRAIN OR VISIONS OF A NEW SCIENCE OF CONSCIOUSNESS
Sam Parnia a) *
Peter Fenwick b)
a) Department of Medical
Specialities, Southampton General Hospital, Tremona Road, Southampton SO
16 6YD, UK
b) The Institute of Psychiatry, London, UK
Abstract
Very little is known about the dying process and in particular the state
of the human mind at the end of life. Cardiac arrest is the final step
in the dying process irrespective of cause, and is also the closest
physiological model of the dying process. Recent studies in cardiac
arrest survivors have indicated that although the majority of cardiac
arrest survivors have no memory recall from the event, nevertheless
approximately 10% develop memories that are consistent with typical near
death experiences. These include an ability to ‘see’ and recall specific
detailed descriptions of the resuscitation, as verified by resuscitation
staff. Many studies in humans and animals have indicated that brain
function ceases during cardiac arrest, thus raising the question of how
such lucid, well-structured thought processes with reasoning and memory
formation can occur at such a time. This has led to much interest as
regards the potential implications for the study of consciousness and
its relationship with the brain, which still remains an enigma. In this
article, we will review published research examining brain physiology
and function during cardiac arrest as well as its potential relationship
with near death experiences during this time. Finally, we will explore
the contribution that near death experiences during cardiac arrest may
make to the wider understanding of human consciousness. © 2002 Elsevier
Science Ireland Ltd. All rights reserved.
Keywords
Cardiac arrest; Near death
experiences; Dying brain; Visions of a new science
1. Introduction
The dying process, and in particular the subjective experience of
dying is an area of which very little is known and, until now, has been
largely ignored by scientific investigation. However, recent studies in
cardiac arrest patients have begun to shed some light on the likely
experiences that we may have at the end of our lives. Certainly from a
clinical point of view, the question of what our patients’ experience
when they face death, is a very real and important issue with everyday
practical relevance. Knowledge of this process may help doctors and
other carers deal with the anxieties of patients who face death.
In this review we will examine the evidence related to the state of the
human mind at the point of death, as well as its potential contribution
in the wider attempts to understand the nature of human consciousness.
The advent of modern resuscitation techniques has enabled many
critically ill patients who would otherwise have died, to be
resuscitated successfully. Some of these survivors have recalled unusual
experiences from their period of critical illness. In 1975 an American
doctor, Raymond Moody, published a best selling book in which he
collected the experiences of 150 people who had been close to death [1].
Recurring features in their accounts included seeing a tunnel, a bright
light, deceased relatives, a mystical being, entering a new domain,
reaching a point of no return, a review of their lives as well as ‘out
of body experiences’ in which people described a feeling of separation
from their bodies and being able to watch themselves as if from a
vantage point above. These recurring features have been termed near
death experiences (NDEs). Although there have been some reports of
unpleasant, ‘nightmarish’ experiences, the majority who experience NDEs
have described them as very pleasant and say that they are left with no
fear of death and a more spiritual view of life [1]. The experiences are
not confined to adults, and have also been reported in children, who
have often been too young to have any real concept of death or an
afterlife [2–5]. Although reported in most cultures, independent of any
religious faith or after life, there are some cultural differences in
the content of the experience [6–8], and the interpretation of the
experience may reflect religious belief [9]. The phenomenon is
relatively widespread; a Gallup survey in the US in the early 1980s
showed that NDEs have been reported in approximately 4% of people who
have been close to death [10].
2. The proposed mechanisms for the causation of NDEs
The most widely accepted scientific view regarding the causation of
NDEs, is that they are either due to a disturbance of brain chemistry
occurring during the dying process or are a psychological response to
the perceived threat of death [11,12]. Many physiological and
pharmacological cerebral mediators have been proposed to account for
NDEs. These include endorphins [13,14], cerebral hypoxia [15],
hypercarbia [11,16], various drugs, in particular hallucinogenic agents
such as ketamine and phencyclidine [17], the NMDA receptor [17],
serotonin pathways [18], activation of the limbic system [19,20], and
temporal lobe anoxic seizures [21].
Thus NDEs are proposed to arise as a form of complex hallucinatory
process in response to either an alteration in cerebral mediators or
even possibly as a psychological form of ‘wish fulfilment’ in response
to the perceived threat of death [22].
3. Cardiac arrest: the closest model to the dying process
Most of the collected data on NDEs have been obtained from
retrospective cases, that have been reported by patients, often many
years after a critical illness or a close encounter with death such as
an accident. The authors have examined more than 750 [23] retrospective
NDE cases, and have found that in most cases it is difficult to
correlate the physiological state of the patients with their experiences
to ascertain exactly how close to death they had been. Physiologically
and clinically, a cardiac arrest is the closest state to the dying
process [24], and in objective terms therefore, experiences arising
during a cardiac arrest shed most light on the state of the human mind
at the point of death. Cardiac arrest is also the most appropriate
condition to study the dying process as, irrespective of cause, it is
the inevitable final stage before death.
During a cardiac arrest the clinical criteria of death are always
reached for a variable length of time ranging from a few seconds to tens
of minutes. By definition, patients have at least two out of the three
criteria of clinical death (no cardiac output, no respiration) and also
usually develop the third (fixed dilated pupils) rapidly with the loss
of brainstem function1.
4. Experimental studies of NDE in cardiac arrest
Recently, a number of independent studies have confirmed reports of
NDEs occurring in cardiac arrests. A 1-year prospective study of cardiac
arrest survivors carried out by the authors showed a 6% incidence of
NDEs [24]. This study, which was based upon interviewed accounts
obtained from in hospital cardiac arrest survivors within 1 week of the
arrest did not find any evidence to support the role of drugs, hypoxia,
hypercarbia or electrolyte disturbances in the causation of NDE. This
was a small study with a total of four out of 63 cardiac arrest
survivors reporting NDEs. In a much larger study just completed in
Holland, 344 cardiac arrest survivors from 10 hospitals were interviewed
over a 2-year period, and 41 or 12% reported a core NDE [25]. Patients
were followed up for a further 8
years following the arrest and reported less fear of death and a more
spiritual outlook on life. The authors of both studies have raised
questions regarding how lucid, well structured thought processes,
together with long term memory formation that is characteristic of NDEs
can arise during a cardiac arrest when cerebral function is impaired and
would not be expected to support lucid thought processes and memory
formation. This can be better understood by examining cerebral
physiology during and after cardiac arrest.
1) It must be
pointed that atropine and epinephrine (adrenaline) which are often
administered in cardiac arrests may cause dilated pupils that appear to
be fixed. However in a cardiac arrest, brainstem activity is rapidly
lost which would lead to the loss of papillary reflexes irrespective of
any administered drugs. The administration of morphine in patients with
myocardial infarction may make the interpretation of pupil size more
difficult.
5. Cerebral physiology during cardiac arrest
There is extensive literature available on the physiology of cardiac
arrest obtained from both human and animal studies. Immediately
following a cardiac arrest due to the cessation of the heartbeat, the
blood pressure drops to immeasurable levels. During properly performed
chest compressions, the systolic pressure may rise to 60–80 mmHg, but
despite this, the diastolic values and hence the mean arterial pressure
still remains low. [26] In one animal study the mean arterial pressure
(MAP) following cardiac arrest was recorded to fall to less than 30 mmHg
(lowest measurable value in this study) and rose only marginally to
approximately 30–40 mmHg during chest compressions [27].
The use of vasopressors such as epinephrine and vasopressin has been
shown to increase blood pressure, and cardiac and cerebral perfusion
pressure compared with chest compressions alone. In one study carried
out in ten humans with prehospital cardiac arrest it was shown that
during CPR epinephrine led to an increase in systolic arterial blood
pressure from 47 (_5) before its administration, to 69 (_7), 74 (_8) and
85 (_8) mmHg with increasing doses of 1, 3 and 5 mg. The diastolic
pressure also increased from 18 (_2) to 27(_3), 25 (_4) and 36(_6) mmHg
respectively but still remained relatively low compared with pre cardiac
arrest levels [28]. Coronary and cerebral perfusion rely on adequate
diastolic and mean pressures and therefore the pressures generated
during cardiac arrest with chest compressions combined with epinephrine,
although better than no intervention, are still generally too low for
adequate perfusion. Other studies in humans have shown similar changes
in blood pressure during the administration of epinephrine and chest
compressions [29]. Cerebral perfusion pressure (CPP) is determined by
the difference between the mean arterial pressure and the intracranial
pressure (MAP–ICP). It has been shown that the more prolonged the
cardiac arrest, the higher the ICP rises and hence a higher MAP is
needed to maintain CPP. In one animal study, cardiac arrest was induced
by ventricular fibrillation in 14 cats. Following 15 min of cardiac
arrest they were then resuscitated using chest compressions together
with the administration of high dose (0.2 mg/kg) epinephrine for 4 min
prior to defibrillation. After restoration of spontaneous circulation
(ROSC) mean arterial pressure stabilised at 80–100 mmHg with
epinephrine. Prior to the induction of cardiac arrest the mean arterial
pressure was 107 (_26). Following 2 and 4 min of chest compressions and
the administration of high dose epinephrine the mean arterial pressure
was 77 (_20) and 65 (_18) mmHg, respectively. There was also a
corresponding cerebral perfusion pressure drop from a prearrest value of
101 (_26), to 37 (_20) and 31(_ 20) mmHg, respectively [30]. In clinical
practice it is generally accepted that a CPP of 70 mmHg is needed for
adequate cerebral perfusion. These relatively low mean arterial blood
pressures are maintained until the resumption of cardiac output despite
conventional cardiopulmonary resuscitation [27–29,31].
In clinical practice the electroencephalogram is often used to assess
cerebral ischaemia during procedures such as cardiac and neurosurgery.
EEG has also been used in assessing cerebral function during cardiac
arrest in animals and humans. The data from humans is largely limited to
those obtained during defibrillation threshold testing at defibrillator
implantation or individual case reports from patients, who were
connected to an EEG during their cardiac arrest. Concurrent EEG
monitoring during a cardiac arrest has shown an initial slowing of the
EEG waves which then progress to an isoelectric (flat) line within
approximately 10–20 s and remain flat during the cardiac arrest until
the resumption of cardiac output in patients after early defibrillation
[31]. In cases of prolonged cardiac arrest EEG activity may not return
for many hours after cardiac output has been returned. In one study of
cardiac arrest in dogs, 15 min of VF cardiac arrest was induced in three
groups of dogs. At the end of the 15 min dogs in the first group were
then treated with conventional cardiopulmonary resuscitation including
closed chest compressions, epinephrine, sodium bicarbonate, and
defibrillation for 3 min before being switched to femoral vein–femoral
artery bypass (F–F bypass). Following the initial 15 min of VF cardiac
arrest dogs in group 2 were given 8 min of conventional cardiopulmonary
resuscitation including defibrillation and epinephrine, before being
connected to F–F bypass. In this group cerebral and myocardial blood
flow was measured during the resuscitation period. In group 3, F–F
bypass was commenced after the initial 15 min cardiac arrest period
together with the other measures including defibrillation and
epinephrine.
In group 1 and 3 EEG measurements were made throughout the resuscitation
period. In group 1 the EEG flattened 21.1_5.7 s (n=10) after VF and
remained flat until 90.0_24.7 min after the start of resuscitation when
bursts of slow waves (burst and suppression) appeared. During the
observation period, interrupted slow waves became continuous waves at
130.7_28.1 min after beginning resuscitation. In group 3, EEG flattened
after 17.4_3.0 s after the occurrence of VF. Burst suppression appeared
62.8_11.6 min and continuous waves appeared at 145.6_27.5 min after the
beginning of bypass. In group 2, local cerebral
blood flow (CBF) decreased rapidly to zero after VF. Myocardial blood
flow also decreased but took approximately 1–2 min to reach zero. After
15 min of cardiac arrest no appreciable local CBF could be restored in
the following 8 min by cardiopulmonary resuscitation including closed
chest compression, ventilation and the administration of resuscitative
drugs. Blood flow returned to pre VF levels following the initiation of
F–F bypass [32]. Therefore, during cardiac arrest cerebral blood flow is
severely impaired which leads to a lack of electrophysiological activity
in the cortex. This is made worse as the period from initial ischemia to
adequate resuscitation is increased. Studies in animals have
demonstrated that an absence of cortical activity as measured by EEG
correlates with an absence or reduction in activity of the deep brain
structures as measured by in-dwelling electrodes [33,34]. As a result of
these processes during a cardiac arrest cerebral function and therefore
consciousness are lost.
6. Cerebral physiology after cardiac arrest
Under normal circumstances the brain receives 15% of the cardiac
output (750 ml/min). The grey matter flow is 60–70 ml/min and the white
matter flow is 25 ml/min. Oxygen and glucose are needed to maintain
cellular integrity (40–50% of total CBF) and electrophysiological
activity (50–60% of CBF) [35]. Although, there is minimal blood flow to
the brain during a cardiac arrest, it has also been shown that local
cerebral blood perfusion is also severely impaired after the restoration
of an adequate blood pressure and gross cerebral blood flow rate. This
is due to local increases in vasoconstriction possibly brought about by
an imbalance in the local production of vasoconstrictors and
vasodilators, explaining the observed lack of EEG electrical activity
despite the maintenance of adequate
blood pressure during the recovery phase of cardiac arrest. In the above
experiment EEG activity did not begin to recover until approximately 63
min after beginning F–F bypass. Immediately after resuscitation there is
a period of multifocal no-reflow (phase 1). This is followed by
transient global hyperaemia lasting 15– 30 min (phase 2). Thereafter
cerebral blood flow becomes severely reduced while cerebral metabolic
rate of oxygen gradually recovers. This is termed the delayed
hypoperfusion phase (phase 3). After 24 h, cerebral blood flow and
metabolism may be restored, remain low or there may be secondary
hyperaemia (phase 4). Multifocal no-reflow is a phenomenon observed in
animals following recovery from cardiac arrest, in which, despite the
restoration of adequate blood pressure, multiple areas of the brain
develop perfusion defects that range from a pin hole to up to 95% of the
brain.
The cerebral hypoperfusion phase is characterised by a decrease in
cerebral blood flow to about 50% or less of normal, but the reduction in
flow is not homogenous in the brain with certain areas having more
reduction in flow compared with other areas. In one animal study in rats
it was shown that the flow rates in the frontal cortex were 10–15% of
control compared with 70–90% in the cerebellum. The main factor
responsible for this reduced cerebral blood flow following a cardiac
arrest is the initial period of ischaemia prior to adequate
resuscitation [35].
From a clinical point of view these observations are supported by the
loss of brain stem reflexes such as the gag reflex that allows patients
to be intubated easily.
These also indicate a loss of brainstem function and perfusion which may
result from depression of the reticular activating system (RAS) that
normally drives cortical function via the thalamus.
7. Interpreting NDE in cardiac arrest
The occurrence of lucid, well structured thought processes together
with reasoning, attention and memory recall of specific events during a
cardiac arrest (NDE) raise a number of interesting and perplexing
questions regarding how such experiences could arise. These experiences
appear to be occurring at a time when cerebral function can be described
at best as severely impaired, and at worst absent. Although, under other
clinical circumstances in which the brain is still functioning, it may
be possible to argue that the experiences may arise as a hallucination
in response to various chemical changes in the brain, this becomes far
more difficult during a cardiac arrest. NDE in cardiac arrest appear
different to hallucinations arising from metabolic or physiological
alterations, in that they appear to occur in a non-functioning cortex,
whereas hallucinations occur in a functioning cortex. Therefore, it is
difficult to apply the same arguments for their occurrence. In addition
cerebral localisation studies have indicated that thought processes are
mediated through a number of different cortical areas, rather than
single areas of the brain. Therefore a globally disordered brain would
not be expected to produce lucid thought processes.
From a clinical point of view any acute alteration in cerebral
physiology such as occurring in hypoxia, hypercarbia, metabolic, and
drug induced disturbances and seizures leads to disorganised and
compromised cerebral function [36]. Furthermore, as already described,
any reduction in cerebral blood flow leads to impaired attention and
higher cerebral function. A recent study by Marshall and co workers has
demonstrated that deterioration in higher cerebral function correlates
with reduction in the levels of cerebral blood flow, and that even
relatively minor reductions in blood flow leads to impaired attention
[37]. NDEs in cardiac arrest are clearly not confusional and in fact
indicate heightened awareness, attention and consciousness at a time
when consciousness and memory formation would not be expected to occur.
An alternative explanation is that NDEs reported from cardiac arrests,
may actually be arising at a time when consciousness is either being
lost, or regained rather than during the actual cardiac arrest period
itself. Experiments during simple fainting episodes have shown that,
experiences arising during loss of consciousness occur in conjunction
with mental experiences at the beginning of the episode [38]. This is
not seen classically in NDEs. The EEG during fainting show a gradual
slowing of the cerebral rhythms with the appearance of delta activity
before finally, in a minority of cases, the EEG becoming flat [39]. In
cardiac arrest, the process is accelerated, with the EEG showing changes
within a few seconds [40].
Any cerebral insult leads to a period of both anterograde and retrograde
amnesia [41,42]. In fact memory is a very sensitive indicator of brain
injury and the length of amnesia before and after unconsciousness is an
indicator of the severity of the injury [43]. Therefore, events that
occur just prior to or just after loss of consciousness would not be
expected to be recalled. Recovery following a cerebral insult is
confusional [41,42]. As has been described above, cerebral function as
indicated by EEG has, in many cases been shown
not to return until many minutes or even a few hours after successful
resuscitation. Despite these observations it can still be argued that
the occurrence of some of the features of an NDE such as seeing a light
or a tunnel potentially may occur during the recovery phase following a
cardiac arrest, with the patient thinking that the experiences had
occurred during the actual period itself. However, anecdotal reports of
patients being able to ‘see’ and recall detailed events occurring during
the actual cardiac arrest, such as specific details
relating to the resuscitation period verified by hospital staff, simply
cannot be explained in this way. For this memory to take place, a form
of consciousness would need to be present during the actual cardiac
arrest itself.
8. NDE in cardiac arrest: clinical conclusions and the potential
contribution to the wider debate on the nature of human consciousness
Patient’s experiences from cardiac arrests have begun to shed some
light on the probable state of the human mmind at the end of life.
Although, as might be expected from studies of cerebral function during
cardiac arrest, the majority of people who survive cardiac arrest recall
no experiences from the period of unconsciousness, there is a
significant proportion who recall unusual experiences that are
characteristic of NDEs. These experiences are generally pleasant and
have positive life mchanging effects on the individual [25]. The
majority of patients with NDEs find it difficult to discuss their
experiences with caregivers as well as family and close friends.
Physicians and other caregivers therefore mshould be aware of these
phenomena and advise patients accordingly. Interestingly, there are a
small proportion of cardiac arrest survivors who have reported being
conscious and aware of events during resuscitation and have recalled
‘seeing’ specific details that would not have been known to them. These
experiences have been recalled, while cerebral function has, through
many studies, been shown to be severely compromised and electrical
activity in both the cerebral cortex and the deeper structures of the
brain have been shown to be absent. From a scientific point of view, the
occurrence of these experiences would therefore seem highly improbable
and paradoxical. However, the fact that they do occur, raises some
questions regarding our current views on the nature of human
consciousness and its relationship with the brain. Editorials in recent
years, including some in ‘Scientific American’ and ‘Nature Neuroscience’
have highlighted the difficulties faced by cognitive neuroscience in
attempting to answer questions regarding the nature and the mechanism by
which subjective experiences and sense of consciousness may arise
through cellular processes [44–46]. Traditionally, it has been argued
that thoughts or consciousness; are produced by the interaction of large
groups of neurones or neural networks [47]. Evidence for this view has
come from the clinical observation that specific changes in function
such as personality or memory are associated with specific cerebral
lesions such as those that occur after head injury. This is further
supported by the results of cerebral localisation studies using
functional MRI and PET scanning, in which specific areas of the brain
have been shown to become metabolically active in response to a thought
or feeling [48]. However, those studies, although providing evidence for
the role of neuronal networks as an intermediary for the manifestation
of thoughts, do not necessarily imply that those cells also produce the
thoughts [49]. Although, undoubtedly complex these networks nevertheless
are composed of individual neurones connected via synapses and various
neurotransmitters that lead to the generation of action potentials
across the cell membrane.
With our current scientific understanding a neurobiological mechanism to
explain how cerebral chemical and electrical processes may lead to
subjective experiences has yet to be discovered [44,45]. Direct evidence
of how neurones or neural circuits can produce the subjective essence of
the mind and thoughts is currently lacking and provides one of the
biggest challenges to neuroscience [50]. Alternative scientific views
for the causation of consciousness and subjective phenomenon have,
therefore, been proposed. These range from the view that consciousness
may arise from ‘quantum’ processes within neuronal microtubules [51], to
consciousness being a form of ‘morphic resonance’ [52] or the
possibility that the mind or consciousness may actually be a fundamental
scientific entity in its own right irreducible to anything more basic
[50,53]. This concept has been proposed to be similar to the discovery
of electromagnetic phenomenon in the 19th century, or quantum
mechanics in the 20th century, both of which were inexplicable in terms
of previously known principles and were introduced as fundamental
entities in their own right [50]. An extension of this has been the view
that contrary to popular perception, what has traditionally been
perceived as spirituality, is therefore also an objective branch of
knowledge with its own laws, theorems and axioms [53].
If the occurrence of NDEs during a cardiac arrest, when the mind (the
collection of all our thoughts, feelings and emotions) and consciousness
(self awareness) appear to continue at a time when the brain is
non-functional and clinical criteria of death have been reached, can be
proven objectively through large studies, then this will lend some
support to this view.
Although at present, this remains a mere possibility, if investigated
through appropriate studies it may have significant implications not
only for medicine but also for society as a whole. Such studies are
currently possible, and it has been proposed to test the claims of
‘consciousness’ and being able to ‘see’ during cardiac arrest
objectively by use of hidden targets that are only visible from a
vantage point above. Although, at first these suggestions may sound
rather unconventional. The study of consciousness has itself for many
years been thought of as unconventional, but has now become a
significant point of debate in neuroscience. Therefore, a new way of
thinking may be needed to provide an insight into understanding this
intriguing, yet largely undiscovered area of science.
_________
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Received 1 July 2001;
accepted 14 September 2001
Resuscitation 52 (2002)
5–11
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* Corresponding author. Tel.: +44-2380-777222x3308; fax: +44-
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