The initial responses to stressors varied, but the stages from cessation of consciousness and respirations through vascular collapse to asystole were remarkably similar ( 3- 5). A wide range of stressors was used in these studies, including hypoxic and anoxic models and rapid bleeding. Over a brief period of pulselessness, reversal became less and less likely, then impossible after 10–15 minutes. Once pulselessness occurred, early administration of chest compressions and epinephrine restored circulation. It generally reversed with the elimination of the insult and restoration of breathing during stages with a pulse and blood pressure ( 2). The reversible period, which is clinical death, was initiated through a pulmonary or central nervous system (CNS) insult. Since 1906, animal studies on resuscitation have revealed a similar pattern. After brain and lungs failed, a period of maintained circulatory and cardiac activity included a change in heart rate and mechanism, with a wide range of bradycardic rhythms emerging blood pressure changed in less than one minute from normal to hypotension and then to pulselessness with loss of electrical cardiac activity over the next several minutes. Clinical observation as the patients declined demonstrated a period of compensation that often included tachycardia, tachypnea, and hypertension followed by a shift in consciousness and decrease in ventilatory drive due to the cessation of function of brain and lungs. Studies of ECG changes in humans during and after clinical death, for example, began by 1912 ( 1) shortly after the development of the electrocardiogram (ECG). Some have referred to the reversible period following cessation of respiration and pulse as “clinical death” and the irreversible as “biological death”. It has long been clear that reversal of the process is possible during a brief window of opportunity through artificial maintenance or restoration of the affected vital organ(s). Models that distinguish stages of the dying process have been established for over 100 years. The various patterns of organ failure are delineated and described as mechanisms of dying ( Figure 1). PEA is not primary cardiac arrest, but is, instead, a late stage in a process of dying that most likely began as arrest of brain, lungs and/or the vascular system. The loss of pulse is the initiation of PEA, but pumping continues when assessed by arterial line or echocardiography (so-called pseudo-PEA) and fades over time (minutes) through PEA to asystole. As the organism enters death, the heart continues to pump until the oxygen and metabolic substrates required for cardiac function are sufficiently depleted that hypotension and bradycardia emerge, which is followed by loss of an effective pulse. Typically, the brain and lungs fail in a sequence that may be so closely linked in time that the first organ to fail is often unclear. The vascular system, therefore, should be viewed as a fourth vital system. In contrast, pulseless electrical activity (PEA) emerges with collapse of the vascular system, which is a common version of decompensation but rarely discussed in resuscitation literature. VF, therefore, is primary cardiac arrest the heart causes the vasculature, brain and lungs to fail. In ventricular fibrillation (VF), for example, the process occurs rapidly as the disorganized activity of the fibrillating heart produces cessation of circulation, which in turn causes loss of consciousness and respiratory drive within seconds. Failure to resuscitate the function of the affected primary organ results in cessation of function of the others. The dying process begins with the loss of function of one or more of the three classic vital organs: heart, brain, lungs.
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