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The decision to control a patient's airway during cardiopulmonary resuscitation (CPR) is straightforward. Patients in cardiopulmonary arrest generally are totally unresponsive, and airway techniques can be used without the need for pharmacological adjuncts. Much of the decision making relates to timing and the type of ventilation method to use. These decisions are influenced by the patient's oxygenation status, duration of arrest, expected difficulties with airway control, and operator experience and training. [ABSTRACT FROM AUTHOR]

Since the 1960s, important advances have been made in resuscitation of patients from sudden cardiac death (SCD). Despite these advances, rates of survival to hospital discharge range from only 2 to 30% (generally 5-10%); rates of survival with intact neurological status are even lower (1). Approximately 400,000 out-of-hospital sudden deaths occur in the United States each year (2). These grim statistics point to the importance of prevention in approaching the problem of SCD from a public health standpoint. [ABSTRACT FROM AUTHOR]

The physiology of cardiopulmonary resuscitation (CPR) is complex and changes over time. Becker and Weisfeldt defined three time-sensitive phases of resuscitation: electrical, circulatory, and metabolic (1). Each of these phases is characterized by multiple physiological abnormalities to become more profound and difficult to reverse over time. Beyond the first phase, which can often be corrected by a single intervention (e.g., prompt defibrillation for ventricular fibrillation [VF] or pulseless ventricular tachycardia, and increasing host of challenges develop (e.g., maintaining coronary and cerebral blood flow and pressure, counteracting vasodilatation, cerebral protection, minimize and postresuscitation left ventricular dysfunction). [ABSTRACT FROM AUTHOR]

Resuscitation began in the hospital setting nearly 40 years ago and little has been done since that time to provide a critical evaluation of the process by which resuscitation is performed. Recent regulatory and federal guidelines are forcing hospitals to assess both process and outcome variables to improve the care given to victims of cardiac arrest (CA). The purpose of this chapter is to review process evaluation issues for hospital-based resuscitation programs and to describe the National Registry of Cardiopulmonary Resuscitation (NRCPR) as a tool for enhancing quality improvement and resuscitation science in the hospital. [ABSTRACT FROM AUTHOR]

The concept of "external cardiac massage," first introduced in the early 1960s by Kouwenhoven, Jude, and Knickerbocker (1), includes chest compressions at a rate of 60 to 100 per minute in conjunction with mouth-to-mouth rescue breathing (2). Refinements of standard cardiopulmonary resuscitation (CPR) since its introduction in the 1960s have included increasing the rate of chest compression from 60 per minute to 100 per minute, which research makes little difference in blood flow (3), and recently decreasing the tidal volume of the positive pressure ventilations under certain circumstances (2,4). Elimination of the carotid artery pulse check in the year 2000 guidelines has abolished an unnecessary delay in starting chest compressions by lay rescuers. Yet for many of us, chest compression remains the centerpiece of resuscitation from full cardiopulmonary arrest, and there has been precious little investigation of how to do it properly. [ABSTRACT FROM AUTHOR]

Seriously ill patients often face tragically difficult choices. Commonly, an advanced resuscitative intervention offers a chance of longer life, with a chance, too, of profound suffering. In a given day, all over the world, thousands undergo the procedure of cardiopulmonary resuscitation (CPR), whereas others are placed on a "do not attempt resuscitation" (DNAR) status. In the United States, it has been estimated that approx 100,000 lives may be saved with advanced resuscitation (1). The performance of CPR, however, may conflict with the patient's own desires and may not be in his or her best interest, especially if suffering from a terminally ill condition. It has also been shown that up to 20% of individuals do not wish to be resuscitated (2,3). Decisions concerning CPR are complicated by the fact that often the decision to initiate CPR must be made within seconds by health care providers who generally have very little knowledge about the patient's illness or of any existing advance directives. [ABSTRACT FROM AUTHOR]

The purpose of any clinical trial is to evaluate treatment(s) in an at-risk population. Clinical trial design principles are the same regardless of the setting. Three very readable books that cover fundamentals and specifics of clinical trial design are those by Friedman, Furberg, and DeMets (1); Meinert (2); and Pocock (3). Clinical trial design is much more than inclusion/exclusion criteria, sample size, randomization to treatment arm, and counting endpoints. Defining and monitoring data collection, monitoring and maintaining compliance, and monitoring and reporting potential adverse events are often the most demanding design aspects. [ABSTRACT FROM AUTHOR]

The ultimate goal of cardiopulmonary resuscitation (CPR) is the total reanimation of the cardiac arrest (CA) victim back to their pre-arrest status. Much of what we know and do regarding human CPR is based on animal modeling of the many components of CA and its treatment. Ideally, hypotheses regarding mechanisms of injury caused by arrest and treatments to improve outcome should first be tested in robust preclinical models of this disease followed by clinical testing. Although some aspects of the disease and treatment lend themselves to computational, cell culture, and isolated organ modeling, whole animal experimentation remains the standard for preclinical testing (1-4). To this end, the proper design and use of the preclinical model is crucial to ensure that clinical trials are warranted and optimally designed for ultimate validation of the hypotheses. [ABSTRACT FROM AUTHOR]

A patient with out-of-hospital cardiac arrest (CA) stands little chance for survival without prior organization and preparations for immediate resuscitation. Fortunately, many communities have achieved relative success with resuscitation since the 1970s. In the 1970s, cities such as Seattle and Milwaukee achieved overall survival-to-hospital discharge rates for the subgroup of patients with out-of-hospital ventricular fibrillation (VF) that exceeded 20 to 30% (1,2). Both of these communities used a classic deployment system for out-of-hospital CA that sent a three- to four-member firefighter crew as a neighborhood "first-responder" (FR) followed by a two- (or more) member paramedic ambulance crew. In cases of witnessed collapse in which the patient received immediate basic cardiopulmonary resuscitation (BCPR) by bystanders and presented to paramedics with VF, survival rates in these systems exceeded 40%. This finding was duplicated in several other communities, including the City of Houston Emergency Medical Services (EMS) system after a major restructuring in the 1980s (3). [ABSTRACT FROM AUTHOR]

Permanent brain damage caused by ischemia and reperfusion that results from disease processes such as stroke and cardiac arrest (CA) with resuscitation has been estimated to affect approx 200,000 patients in the United States annually (1). Neuronal damage from stroke and CA occur by different mechanistic models of injury. In ischemic stroke, only a portion of the brain is at risk, and the ischemia is only complete in the center of the vulnerable area. This central area of dense ischemia is surrounded by a penumbral zone in which blood flow is diminished but not completely lost. As opposed to CA with resuscitation, flow ceases altogether and the entire brain is at risk for a transient period of complete ischemia followed by reperfusion (2). [ABSTRACT FROM AUTHOR]

Cardiovascular disease remains the most common cause of disease-related death in the United States, resulting in approx 1 million deaths per year. It is estimated that 400,000-460,000 Americans will die from cardiac arrest (CA) each year, nearly 90% in prehospital settings (1,2). Data regarding the incidence of unexpected childhood cardiopulmonary arrest (CPA) is less robust, but the best recent data suggest that approx 16,000 American children suffer a CA each year with an annual incidence of roughly 20 out of 100,000 children (3,4). [ABSTRACT FROM AUTHOR]

Real strides have been made in the last decade in the treatment of sudden cardiac death. Survival rates from out-of-hospital cardiac arrest (CA) have been reported as low as 1 and 2% in large cities (1,2). Communities with rapid emergency response teams have reported better results with survival rates from 15 to 30% (3). Within the last few years providing early defibrillation by equipping nonmedical first responders with automated external defibrillators (AEDs) has been a crucial step in improving survival from out-of-hospital CA. Recent reports from Rochester, Minnesota, where police are now providing early defibrillation, have shown a community-wide survival rate of 40% for patients whose initial rhythm is ventricular fibrillation (VF [4]). Casinos in which security personnel were trained to use AEDs have reported overall survival rates from VF of 59% for victims of sudden CA on property (5). Similarly, the Chicago Airport Authority experience has been impressive (6,7). After placing AEDs in the terminals of both O'Hare and Midway airports, they found a 56% neurologically normal survival rate for VF CA within the first 24 months of starting this public access defibrillation program. [ABSTRACT FROM AUTHOR]

Shock is a complex entity defined traditionally as a state in which the oxygen utilization or consumption needs of tissues are not matched by sufficient delivery of oxygen. This mismatch commonly results from states of altered tissue perfusion. From this perspective, cardiopulmonary arrest represents the most extreme of shock states. [ABSTRACT FROM AUTHOR]

Cardiopulmonary resuscitation (CPR) in a patient with multiple injuries involves a different approach than in a nontrauma patient. Although the basic principles are the same as dealt with in other chapters of this book, CPR in the trauma victim has to address prevention of cardiopulmonary failure from problems exclusive to the injured patient. This chapter concentrates on these issues and highlights some of the recent developments in the field. [ABSTRACT FROM AUTHOR]

The contemporary allure of hypothermia is regularly sparked by the apparent "reanimations" of profoundly cold patients in prolonged cardiac arrest (CA). Recently, a physician who was resuscitated from 13.7°C presented her own case report at an international conference (1). There are also promising ongoing investigations of mild therapeutic hypothermia for traumatic intracranial hypertension and stroke (2-4). Nevertheless, hypothermia remains more of a geographically and seasonally pervasive physiological threat than a therapy (5-8). [ABSTRACT FROM AUTHOR]

In the past 40 years, lightning has killed more people than any other storm-related phenomena except floods (1). On average, lightning causes 75 to 100 deaths per year (1). The number of nonfatal injuries is estimated to be 10 times the number of deaths, but the exact number is not precisely known because of incomplete reporting (2). A risk table for lightning injury is available at http://www.lightningsafety.noaa.gov and is excerpted as Table 1. [ABSTRACT FROM AUTHOR]

Several definitions and multiple terminology have appeared since the 1950s regarding the description of victims who suffer a fatal or near-fatal event from being submerged in water and other liquids. Some of the descriptors have had modifications placed on them and, furthermore, their meaning was somewhat lost when translated into some languages other then English. Because drowning is a global problem, at the World Congress on Drowning in Amsterdam, The Netherlands, in 2002, a group was convened from multiple countries to develop a definition of "drowning" that would be applicable in multiple languages worldwide (1). Although unanimity may not have been present on every term discussed, there clearly was a consensus to simplify the terminology for international application. What follows is the consensus of that group with comment and, in some cases, slight modification representing the bias of the authors of this chapter. [ABSTRACT FROM AUTHOR]

Cardiac arrest (CA) in pregnancy is an uncommon occurrence with an incidence of about 1 in every 30,000 deliveries (1). The causes are quite numerous, but the management is essentially the same with the exception of a few modifications regarding the fetus. In this chapter, causes of maternal mortality are reviewed along with potential interventions to decrease its incidence. A general overview of maternal and fetal physiology and how it pertains to the resuscitation of the mother will also be provided. Pharmacological agents used in the resuscitative protocol and their effects on the fetus are discussed. Finally, the issue of perimortem cesarean delivery is addressed, along with the difficult questions that must be answered within minutes of deciding who should and should not be considered for this drastic, potentially lifesaving procedure. [ABSTRACT FROM AUTHOR]

Sudden cardiac death (SCD) annually affects 400 to 460,000 individuals in the United States, accounting for half the mortality rate as a result of coronary heart disease. SCD remains a major unresolved public health problem. Pathophysiologically, SCD arises from a harmful interplay of myocardial structure, and function. Structural abnormalities furnish the anatomic substrate for SCD and include the myocardial repercussions of coronary artery disease (CAD), left ventricular hypertrophy (LVH) and/or dilation, and specific electrophysiological anatomic abnormalities. The functional issues capable of destabilizing a chronic electrophysiological abnormality include transient ischemia and reperfusion, systemic issues (e.g., electrolyte disturbances, pH changes, and hemodynamic dysfunction), autonomic fluctuations (both at a systemic and a tissue level), and proarrhythmic effects of various drugs. We center the discussion in this chapter on two aspects of electrolyte abnormalities; first, the role they play in the origin of SCD and second how the therapies employed during cardiopulmonary resuscitation (CPR) can result in specific electrolyte abnormalities. Cardiopulmonary arrest (CPA) can occur in a wide spectrum of patient types, some with underlying cardiac abnormalities receiving active treatment others without any obvious cardiovascular (CVR) malady. It is in the instance of the former that electrolyte disturbances can precede and on occasion incite a CPA (1). Such electrolyte abnormalities can have multiple origins, relating to either intercurrent illnesses or administered medications. In most cases those circumstances impacting potassium (K+) and magnesium (Mg++) homeostasis are of most importance. The electrophysiologic basis of CPA can be quite complex and a detailed discussion of the electrophysiologic effects of electrolyte abnormalities extends beyond the scope of this chapter. The reader is directed to several excellent discussions on this topic (1-4). [ABSTRACT FROM AUTHOR]

Cardiac arrest (CA) as a result of poorly tolerated ventricular tachycardia (VT) or ventricular fibrillation (VF) is the most common cause of death in many developed countries including the United States. Even with a steady decline in morbidity and mortality from cardiovascular diseases over 30 years (1), approx 60% of the 489,171 deaths attributable to coronary artery disease (CAD) in 1990 were out-of-hospital CA. In 1998, 63% of cardiac deaths were sudden and likely arrhythmic (2). Many of these deaths could have been prevented if the responsible ventricular arrhythmia had been treated with proper resuscitative efforts. Of 350,000 men who died in 1998, 41% had out-of-hospital sudden death, and 22% had a cardiac death in the emergency department (ED) or were dead on arrival. Of 369,000 women who died that year, 52% had out-of-hospital sudden death, and 12% had a cardiac death in the ED or were dead on arrival (2). [ABSTRACT FROM AUTHOR]

The buffer therapy of acid-base changes during CPR is less controversial than in previous years. Overwhelming experimental and some clinical data failed to demonstrate an improvement in survival after buffer therapy. However, the scant data from randomized controlled trials still impede a clear-cut recommendation on how really to treat cardiopulmonary resuscitation (CPR)-associated acid-base changes. [ABSTRACT FROM AUTHOR]

The importance of vital organ perfusion in patients suffering cardiac arrest (CA) makes arterial vasomotor tone, and the resultant perfusion pressure, critical in resuscitation from sudden death. After failure of countershock, ventilation, and oxygenation, the target organ for resuscitative pharmacotherapy becomes the arterial vascular smooth muscle cell. Selective stimulation of various vascular smooth muscle cell surface receptors is accomplished through administration of exogenous agents with the intention of altering blood flow away from nonvital organ beds toward the myocardium and brain. [ABSTRACT FROM AUTHOR]

The primary goal of cardiopulmonary resuscitation (CPR) is to restore spontaneous circulation and manage postresuscitation myocardial dysfunction, including myocardial contractile failure and life-threatening ventricular ectopic dysrhythmias. During CPR, blood flow is determined primarily by two issues: the pump (driving force) and the peripheral vascular resistance. The mechanical interventions are intended to generate maximal cardiac output and perfusion pressure. A second issue is that of vascular tone. Accumulation of metabolic vasodilator substances, including adenosine, carbon dioxide, lactic acid, and hydrogen ions, and diminished neurovascular vasoconstriction decrease peripheral arterial resistance by causing (or allowing) arterial vasodilation. Additionally, there are variable increases in venous capacitance such that venous return to the right atrium is reduced. This has been the basis for the use of vasopressor agents, especially α-adrenergic agents. Quite distinct, however, is immediate postresuscitation management, which has as a primary goal the mitigation of postresuscitation myocardial failure. Pharmacological interventions are designed to improve myocardial systolic function by increasing stroke volume, reducing ventricular filling pressures, and controlling arrhythmias. [ABSTRACT FROM AUTHOR]

The time from onset of cardiopulmonary arrest until restoration of an effective, spontaneous circulation is the single most important determinant of long-term, neurologically intact survival from cardiopulmonary arrest. Prompt defibrillation of ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), when either rhythm is present, is more likely to alter patient outcome than is immediate pharmacological management (1). However, treatment with pharmacological agents is frequently required in patients with VF or VT that is refractory to electrical countershocks, and in patients with asystole or pulseless electrical activity (PEA). [ABSTRACT FROM AUTHOR]

Cardiopulmonary bypass (CPB) is now 50 years old. Although developed originally to allow correction of congenital and valvular heart disease, CPB has affected all of medicine profoundly. As an artificial circulatory support for systemic and pulmonary functions, CPB has allowed for the development of cardiovascular surgery. Today, coronary artery bypass grafting is the most commonly performed cardiac surgery. The current trend is to perform a larger number of more complicated coronary revascularization surgeries "off pump." However, CPB supported work still accounts for the vast majority of surgeries. The CPB technology has evolved from one with large oxygenators, blood prime, and complex heating and cooling to today's smaller and less complex technologies. [ABSTRACT FROM AUTHOR]

Sudden cardiac death remains a major medical challenge despite the advent of defibrillation decades ago. There are few minutes to defibrillate the heart and thereby stop ongoing ischemic injury to key organs such as the heart and brain, and few therapies proven to protect against the postresuscitation phase of cardiac arrest (CA)—when up to 90% of patients go on to die despite successful defibrillation (2). New approaches are desperately needed to improve CA survival, and the induction of transient hypothermia may be one of the most promising of new approaches (2). Hypothermia used to protect against conditions of low blood flow has historically been induced at different times relative to the arrest (see Fig. 1): pre-arrest, intra-arrest, and postarrest. Pre-arrest cooling is typically induced to as low as 20°C for cardiac surgery and is induced before and simultaneous to the time of arrest. Postarrest cooling to 32 to 33°C was found to be protective in recent human CA trials, induced by applying cooling blankets in the subset of CA patients having return of spontaneous circulation (ROSC) who remained unresponsive (3,4). The goal of this hypothermia was to prevent neurologic injury although maintaining a temperature warm enough to prevent the cardiac and numerous other side effects of more profound cooling (e.g., cardiac arrhythmias, coagulopathies, infections). This cooling was protective despite taking 8 hours to reach target temperature after ROSC (4). Intra-arrest cooling, when cooling is induced after failed initial CPR, has the potential to induce a stasis state for a period of time (i.e., suspended animation) long enough for more definitive circulation (e.g., cardiac bypass) to be established and life restored. Little is known about the optimal depth or clinical potential of such hypothermia, due in large part to the technical difficulties involved in inducing profound hypothermia during the low-flow states of sudden CA. [ABSTRACT FROM AUTHOR]

The incidence of sudden arrhythmic deaths continues to be a significant problem despite the fact that mortality from acute coronary syndromes continues to decrease in response to early interventions and improved secondary prevention (1-3). Most patients with coronary artery disease who suffer cardiac arrest (CA) do not have acute myocardial infarction (AMI [4-6]). Thus, primary arrhythmic causes of CA are becoming increasingly important. [ABSTRACT FROM AUTHOR]

The value of early intervention in critically ill patients has long been recognized. As early as the 1700s, scientists recognized the value of mouth-to-mouth respiration and the medical benefits of electricity (1). In the modern era, advances in resuscitation began to proliferate. In 1947, Claude Beck successfully resuscitated a 14-year-old boy through the use of open chest massage and an alternating current (AC) defibrillator, the kind that is used in wall outlets. In 1956, Paul Zoll demonstrated the effectiveness of closed chest massage with the use of an AC defibrillator. In the late 1950s, Peter Safar, William Kouwenhoven, James Jude and others began to study sudden cardiac arrest (CA) and in 1960, they demonstrated the efficacy of mouth-to-mouth ventilation and closed chest cardiac massage (2). In 1961, Bernard Lown demonstrated the superiority of direct current (DC) defibrillators, the kind provided by batteries. In 1966, J. Frank Pantridge and John Geddes developed the world's first mobile intensive care unit (MICU) in Belfast, Northern Ireland, as a way to bring early advanced medical care to patients with cardiac emergencies (3). In 1969, William Grace established the first MICU in the United States in New York City (4). Subsequently, there were efforts in the United States and throughout the world to emulate and build on this concept. In the late 1960s and early 1970s, paramedic programs were developed by Eugene Nagel in Miami, Leonard Cobb in Seattle, Leonard Rose in Portland, Michael Criley in Los Angeles, and James Warren and Richard Lewis in Columbus. In the 1980s, Mickey Eisenberg, Richard Cummins, and colleagues demonstrated the effectiveness of rapid defibrillation in Seattle, Washington (5), while Kenneth Stults demonstrated the same in rural Iowa (6). This growing body of research demonstrated the importance of rapid care for victims of sudden CA by showing that survival improved when basic life support (mouth-to-mouth ventilation and closed chest compressions) was provided within 4 minutes and advanced life support (defibrillation, intravenous medications and fluids, and advanced airway management) within 8 minutes. Subsequent studies found that the benefits of advanced life support were primarily the result of electrical countershock for patients in ventricular fibrillation (VF). From these findings, a model of care called the "Chain of Survival," was first described by Mary Newman (7), and then by Cummins et al. (8), and eventually adopted by the Citizen CPR Foundation, the American Heart Association (AHA) and others. The Chain of Survival consists of four action steps that must occur in rapid succession to provide the patient the greatest likelihood for resuscitation: early access (call 911 or the local emergency number to notify the emergency medical services [EMS] system and summon on-site help); early cardiopulmonary resuscitation (CPR; begin immediately); early defibrillation; and early advanced care (transfer care to EMS professionals upon their arrival at the scene). [ABSTRACT FROM AUTHOR]

The history of applying electrical shocks to the heart began in the 1700s with direct current derived from a Leyden jar. In 1775, Abildgard described having shocked a chicken into lifelessness and on repeating the shock, bringing the bird back to life (1). Transthoracic defibrillation was first performed clinically in the mid-1950s when Zoll introduced the alternating current (AC) defibrillator (2). Several years later, Lown introduced the direct current (DC) defibrillator as an improvement on Zoll's device in several important areas, specifically that it caused less damage to the patient and that it could be made portable (3). Today, internal cardioverter defibrillators are the size of a small bar of soap and can monitor and correct a patient's rhythm for several years between replacements. Likewise, the external defibrillator has been made smaller and so much simpler to operate that sixth graders can use the device successfully. [ABSTRACT FROM AUTHOR]

Cardiopulmonary resuscitation (CPR) is first-line therapy for sudden, unexpected, cardiac arrest (CA). Laypersons are most likely to administer CPR because most CAs occur in the home or in the community. Training laypersons to adminster CPR has become a routine activity but some would argue that it is not an activity that we do particularly well. Out-of-hospital resuscitation attempts have led to very low survival rates (1-13)—less than 10% survival in Europe (2,3,6-8) and the majority of urban areas in the United States (1,9-13). Densely populated urban areas such as Chicago and New York City have a particularly low rate of sudden CA survival (13) as do rural areas. [ABSTRACT FROM AUTHOR]

The standard technique of external chest compression in cardiopulmonary resuscitation (CPR) has changed little since the landmark paper of Kouwenhoven et al. in 1960 (1). The rhythmic application of force to the body of the patient is fundamental to the process of generating blood flow in CPR, but there is little agreement regarding the optimal technique for applying that force. There is a great need for improved external chest compression techniques, because only an average of 15% of patients treated with standard CPR survive cardiac arrest (CA [2,3]), and it is widely agreed that increasing the blood flow generated by chest compression will improve survival. Given the potential importance of newer devices and techniques that may augment blood flow, this chapter will explore several alternate devices and techniques that have been studied. [ABSTRACT FROM AUTHOR]

Sudden death, mainly out-of-hospital death, is a major public health burden throughout the world. It accounts for 50 to 75% of all fatal cardiovascular disease (CVD) events in countries where data are collected. It is usually unexpected, affecting all age, gender, and ethnic groups (1). The immediate mechanism of death is ventricular fibrillation or ventricular standstill, but the underlying cause is commonly ischemic coronary heart disease (CHD). However, other causes including different forms of cardiac pathology, genetic and environmentally induced, are also well recognized. [ABSTRACT FROM AUTHOR]

In the early resuscitation guidelines, electrical mechanical dissociation (EMD) referred to the prescence of organized electrical activity in the absence of synchronous myocardial contraction (1-3). As such, electrical activity was detected on the surface electrocardiogram but no effective cardiac output was present owing to the absence of coupled mechanical activity. The clinical result was the absence of pulse, blood pressure, and heart tones. EMD was observed in a variety of resuscitation situations and was felt to be secondary to prolonged global cardiac ischemia. The organized rhythm varied from sinus tachycardia with a normal duration QRS complex to brady-dysrhythmias with wide aberrant or idioventricular ventricular morphologies. A poor resuscitation outcome and dismal prognosis was a common shared observation. Collectively, this ominous rhythm was found to have a resuscitation rate of only about 20% and a hospital discharge rate of 4 to 5% (4,5). [ABSTRACT FROM AUTHOR]

Bradyasystole is a term encompassing many different types of rhythms meeting the following definition: any electrical rhythm that has a ventricular rate below 60 beats per minute (bpm) in adults and/or periods of absent heart rhythm (asystole). A bradyasystolic state is a clinical condition in which the predominant cardiac rhythm can be classified as bradyasystole. Bradyasystolic rhythms other than asystole may be accompanied by a pulse. A bradyasystolic rhythm even with a pulse is frequently a precursor to cardiac arrest (CA) and requires prompt intervention. Some of the causes of bradyasystole are the same whether or not a pulse is present. More commonly bradyasystole occurs without a pulse. Bradycardic rhythms without a pulse are one group of many different types of rhythms described as pulseless electrical activity (PEA). [ABSTRACT FROM AUTHOR]

Death by acute airway obstruction has been recognized for centuries. George Washington is thought to have died in 1799 from upper airway obstruction p caused by acute bacterial epiglottitis (1). Although letting of more than 2 L of blood out of their patient, President Washington's physicians apparently discussed performing a tracheotomy, a procedure that had been described in detail only the year before. However, they did not have the courage to carry out the new procedure on the retired president of the United States. Dr. R. K. Haugen wrote a now-classic description of the problem of choking in 1963 (2). He described what he termed the café coronary: A middle-aged or elderly person, at a fashionable restaurant, is partaking of filet mignon, or perhaps broiled lobster or prime rib of beef. At the same time, he is conversing with companions at dinner. Suddenly, he ceases to eat and talk. The dinner companions are perplexed but not alarmed for there is no indication of distress. Then, the person suddenly collapses at the table. [ABSTRACT FROM AUTHOR]

Ventilation—the movement of fresh air or other gas from the outside into the lungs and alveoli in close proximity to blood for the efficient exchange of gases—enriches blood with oxygen (O2) and rids the body of carbon dioxide (CO2) by movement of alveolar gas from the lungs to the outside (1). [ABSTRACT FROM AUTHOR]

Through much of recorded history, resuscitation was forbidden. Although written accounts of resuscitation can be found, it is clear that successful reversal of death was thought to have been performed directly by God or through appointed agents. For example, stories of resuscitation in the Bible involve prophets acting clearly as vessels through which God's power restores life (1,2). In these and other resuscitation accounts, reversal of death was considered the province of God and not something mere mortals should undertake. This "prohibition" against resuscitation was challenged during the Enlightenment, an amazing period of scientific discovery. Starting around 1750, scientists and philosophers questioned the dogma of the past and came to believe that humans could understand and control their own destinies. They wished to discover the workings of the universe as well as the ticking of life itself. To speak of the science of resuscitation one must begin where science begins. And there is no more crucial ingredient to science than the scientific method—a key achievement of the Enlightenment. The intellectual giants of the Enlightenment claimed that the world could best be understood through scientific discovery, and the means to achieve this was the scientific method. [ABSTRACT FROM AUTHOR]