Today, human-made and natural sources together kill about 1100 to 1200 people each year in the United States. The number of people injured worldwide by electricity, however, remains unclear, because it is generally underreported and it is common for survivors to avoid medical care initially. Although scientific investigations of electrical injuries date back to 1884, with current scientific knowledge and the clinical appearance of electrical injuries, we now know that the outcomes of electrical injuries differ substantially, depending on whether technical electricity with low-volt household current, high-volt current, or lightning is the underlying cause.

Injuries after electrocution are often dramatic and potentially fatal. In the majority of victims injuries are caused by the effects of electrical, thermal, and mechanical energy. Secondary trauma may result from falls, explosions, or violent muscle contractions. Cardiac and respiratory arrest may occur immediately or secondary to direct effects of current. Many victims die before advanced life support can be provided, and survivors may suffer permanent disabilities. What is unique about electrical injuries, however, is the potential for good resuscitation outcome even after long arrest times. This may be a result of the electrical shock itself or because these accidents tend to occur in younger persons with few or no underlying pathological conditions.

Considering the magnitude of the voltage and current involved, it is amazing that anyone survives an encounter with a bolt of lightning. Lightning can cause harm by electrical energy (e.g., direct hit, side splash, upward streamer, ground strike, conducted current, step voltage) and can cause trauma (e.g., heat, explosion, fall).

Non-fibrillatory cardiac arrest is a term used to encompass the defined cardiac arrest rhythms, pulseless electrical activity (PEA) and asystole, arrest rhythms that are distinct from ventricular fibrillation or pulseless ventricular tachycardia. Until recently, the term electromechanical dissociation (EMD) was used in place of PEA. EMD was defined as the presence of electrical complexes without accompanying mechanical contractions of the heart. Several studies have demonstrated that often during EMD arrest there actually is mechanical cardiac activity associated with the electrical complexes seen on a cardiac monitor. PEA, defined as organized electrical activity with the absence of clinically detectable pulses, is thus a physiologically more appropriate terminology. Patients in asystole, by definition, have no discernible ventricular activity by electrocardiography or ultrasonography, and no associated perfusion. This chapter will focus on the diagnosis and treatment of PEA subsets.

The incidence of PEA during cardiac arrest appears to be changing. Prior to 1990, PEA was reported to be the initial presenting rhythm in approximately 20% of hospitalized patients who are monitored at the onset of cardiac arrest and 16.5% of patients who present to a prehospital system in cardiac arrest. Several recent studies have reported the incidence of PEA to be 35%–40% of all in-hospital resuscitation events. Data from the Ontario province advanced life support (OPALS) study found over a 4-year study period an increasing PEA incidence of 19.9% to 24.5%, with a coexisting shortened EMS system response time.8 The OPALS group further demonstrated a 50.1% incidence of PEA arrests in the subgroup of patients that arrested after the arrival of EMS.

Although asphyxia literally means no pulse (in Greek), it represents an inability to breathe and therefore suffocation. Failure of gas exchange is characterized by hypoxemia and hypercarbia, as originally defined by J.B.S. Haldane. A mechanistic classification of asphyxia (Table 55.1) includes a diversity of pathophysiological processes that preclude movement of gas from the upper airway to the alveoli and ultimately to the tissues, the cells, and then to the mitochondria, thereby sustaining oxidative metabolism in vital organs.

Asphyxia is a cause of sudden death, but in contrast to primary cardiac causes, it more often presents with bradycardia and asystole rather than ventricular fibrillation (VF). In children, normothermic cardiac arrest is predominantly due to asphyxia. Asphyxia is also the predominant mechanism of cardiac arrest in neonates and in infants due to the so-called sudden infant death syndrome, Status asthmaticus is an important cause of asphyxia. The most frequent cause is failure of respiratory muscle function. Outcomes are worsewhenVF evolves during asphyxial cardiac arrest than after primary VF in adults.

Anoxia or hypoxia is defined by critical reductions in arterial oxygen saturation (SaO2) or arterial oxygen tension (PaO2). Hypercarbia is defined by increases in arterial carbon dioxide tension (PaCO2) in settings of inadequate alveolar ventilation and usually in association with hypoxia.

Introduction

Cardiac arrest from poisoning results from direct effects on the cardiovascular or the central nervous system (CNS). Cardiac effects may be caused by perturbation of the autonomic system, antagonism of ion channels, or interference with myocardial metabolism. CNS active poisons cause cardiac arrest through either respiratory suppression (leading to asphyxial arrest) or CNS stimulation with seizures or severe agitation (and the resultant metabolic abnormalities). Restoration of hemodynamics often requires addressing the effects of the poisoning in addition to standard treatment of cardiac arrest.

There are very few studies of specific treatment for cardiac arrest from poisoning. The utility of some interventions, such as ensuring ventilation and oxygenation for patients with cardiac arrest due to CNS depressants, is selfevident. The last two ACLS updates include a section on the treatment of cardiac arrest from poisoning. This section was a major advance in that it recognized that cardiac arrest from poisoning is a unique situation, but it also highlighted the lack of quality data in this area. If studies of naloxone are excluded, the recommendations are based on fewer than 500 patients, and most of these data are anecdotal. A few interventions have been studied systematically in animal models of severe poisoning, but there are no systematic animal studies of therapy for cardiac arrest. Given the lack of systematic data, the treatment of cardiac arrest remains more art than science, and the standard of care is poorly defined except for initial supportive care. The recommendations in this chapter are a guide to clinicians, but they should not be considered as standard of care.

There is a no more frightening experience for a clinician than a patient's sudden and complete loss of vital signs. The need to initiate multiple complex therapies, all the while knowing that each minute that passes dramatically decreases the chances for a good outcome, makes sudden death the penultimate medical emergency.

Premature death is the adversary of physicians. For millennia, the loss of life signs was considered the victory of death. Students were taught that once patients had succumbed they were beyond the healing arts. Only relatively recently have physicians regularly attempted to wrest such patients back from death.

Accurate numbers are difficult to obtain. It is said that more than 300,000 persons die each year from sudden cardiac death in the United States alone. Worldwide the figure is in the millions. Sudden death is not, however,caused by coronary artery disease alone. Hemorrhage and asphyxiation, among others, can kill physiologically competent patients without warning. Sudden death is not defined by etiology; it is the circumstance of cardiopulmonary arrest in a person with functional vital organ systems. It is death in the midst of life, and it is always tragic.

We are just beginning to appreciate the magnitude of this problem and the potential for therapy. Just a 5% improvement in outcome – something that could be achieved in many communities by better application of standard care – would save more lives than therapies that have received far more attention. The potential for good is astounding; the relationship of cost to benefit compelling.