5. NEUROPHYSIOLOGY IN CARDIAC ARREST
All these elements of an NDE were experienced during the period of cardiac arrest, during the period of apparent unconsciousness, during the period of clinical death! But how is it possible to explain these experiences during the period of temporary loss of all functions of the brain due to acute pancerebral ischemia?
We know that patients with cardiac arrest are unconscious within seconds. But how do we know that the electroencephalogram (EEG) is flat in those patients, and how can we study this? Complete cessation of cerebral circulation is found in cardiac arrest due to ventricular fibrillation (VF) during threshold testing at implantation of internal defibrillators. This complete cerebral ischemic model can be used to study the result of anoxia of the brain.
In VF complete cardiac arrest occurs, with complete cessation of cerebral flow, resulting in acute pancerebral anoxia. The middle cerebral artery blood flow, Vmca, which is a reliable trend monitor of the cerebral blood flow, decreases to 0 cm/sec immediately after the induction of VF.17 Through many studies in both human and animal models, cerebral function has been shown to be severely compromised during cardiac arrest, and electrical activity in both cerebral cortex and the deeper structures of the brain has been shown to be absent after a very short period of time. Monitoring of the electrical activity of the cortex (EEG) has shown that ischemia produces a decrease of power in fast activity and in delta activity and an increase of slow delta I activity, sometimes also an increase in amplitude of theta activity, progressively and ultimately declining to isoelectricity. More often initial slowing and attenuation of the EEG waves is the first sign of cerebral ischemia. The first ischemic changes in the EEG are detected an average of 6.5 seconds after circulatory arrest. With prolongation of the cerebral ischemia, progression to isoelectricity occurs within 10 to 20 (mean 15) seconds from the onset of cardiac arrest.18-21
After defibrillation the Vmca, measured by transcranial Doppler technique, returns rapidly within 1-5 seconds after a cardiac arrest of short duration. However, in the case of a prolonged cardiac arrest of more than 37 seconds, the Vmca shows an initial overshoot upon reperfusion, a transient global hyperaemia, followed by a significant decrease in cerebral blood flow up to 50% or less of normal.22 This results also in an initial overshoot of cerebral oxygen uptake (hyperoxia) with a fast decrease in cerebral oxygen uptake to borderline values for a considerable time due to delayed hypoperfusion.18,22 In the case of a prolonged cardiac arrest the EEG recovery also takes more time, and normal EEG activity may not return for many minutes to hours after cardiac function has been restored, depending on the duration of the cardiac arrest, despite maintenance of adequate blood pressure during the recovery phase. Additionally, EEG recovery underestimates the metabolic recovery of the brain, and cerebral oxygen uptake may be depressed for a considerable time after restoration of circulation.18 In acute myocardial infarction the duration of cardiac arrest (VF) in the Coronary Care Unit (CCU) is usually 60-120 seconds, on the cardiac ward 2-5 minutes, and in out-of-hospital arrest it usually exceeds 5-10 minutes. Only during threshold testing of internal defibrillators or during electrophysiological stimulation studies will the duration of cardiac arrest rarely exceed 30-60 seconds.
Anoxia causes loss of function of our cell systems. However, in anoxia of only some minute’s duration this loss may be transient; in prolonged anoxia cell death occurs, with permanent functional loss. During an embolic event a small clot obstructs the blood flow in a small vessel of the cortex, resulting in anoxia of that part of the brain, with loss of electrical activity. This results in a functional loss of the cortex like hemiplegia or aphasia. When the clot is dissolved or broken down within several minutes the lost cortical function is restored. This is called a transient ischemic attack (TIA). However, when the clot obstructs the cerebral vessel for minutes to hours, it will result in neuronal cell death, with a permanent loss of function of this part of the brain, with persistent hemiplegia or aphasia, and the diagnosis of cerebrovascular accident (CVA) is made. So transient anoxia results in transient loss of function.
In cardiac arrest global anoxia of the brain occurs within seconds. Timely and adequate CPR reverses this functional loss of the brain, because definitive damage of the brain cells, resulting in cell death, has been prevented. Long lasting anoxia, caused by cessation of blood flow to the brain for more than 5-10 minutes, results in irreversible damage and extensive cell death in the brain. This is called brain death, and most patients will ultimately die.
From these studies we know that in our prospective study1 as well as in the other studies2,3 of patients who have been clinically dead (VF on the ECG), total lack of electric activity of the cortex of the brain (flat EEG) must have been the only possibility, but also the abolition of brain-stem activity, such as the loss of the corneal reflex, fixed and dilated pupils, and the loss of the gag reflex, is a clinical finding in those patients. However, patients with an NDE can report a clear consciousness, in which cognitive functioning, emotion, sense of identity, and memory from early childhood was possible, as well as perception from a position out and above their “dead” body. Because of the occasional and verifiable out-of-body experiences, like the one involving the dentures in our study,1 we know that the NDE must happen during the period of unconsciousness, and not in the first or last seconds of this period. There is also a well documented report of a patient with constant registration of the EEG during surgery for an gigantic aneurysm at the base of the brain, operated with a body temperature between 10 and 15 degrees Celsius. She was connected to a heart-lung machine, with VF, with all blood drained from her head, with a flat line EEG, with clicking devices in both ears, with eyes taped shut, and this patient experienced an NDE with an out-of-body experience, and all details she perceived and heard could later be verified.15
So we have to conclude that NDE in our study,1 as well as in the American2 and the British study,3 was experienced during a transient functional loss of all functions of the cortex and of the brainstem. How could a clear consciousness outside one’s body be experienced at the moment that the brain no longer functions during a period of clinical death, with a flat EEG? Such a brain would be roughly analogous to a computer with its power source unplugged and its circuits detached. It couldn’t hallucinate; it couldn’t do anything at all. As stated before, up to the present it has generally been assumed that consciousness and memories are localized inside the brain, that the brain produces them. According to this unproven concept, consciousness and memories ought to vanish with physical death, and necessary also during clinical death or brain death. However, during an NDE patients experience the continuity of their consciousness with the possibility of perception outside and above one’s lifeless body. Consciousness can be experienced in another dimension without our conventional body-linked concept of time and space, where all past, present and future events exist and can be observed simultaneously and instantaneously (non-locality). In the other dimension, one can be connected with the personal memories and fields of consciousness of oneself as well as others, including deceased relatives (universal interconnectedness). And the conscious return into one’s body can be experienced, together with the feeling of bodily limitation, and also sometimes the awareness of the loss of universal wisdom and love they had experienced during their NDE.