Nearly 200 years of effort and experimentation aimed at finding an effective method of artificial respiration culminated in the work of Archer Gordon in 1949. To compare various methods of artificial respiration, Gordon spent 1 year, with no salary and no funding, in Cook County Hospital, Chicago, where he was on call 24 hours/day. His experimental procedure consisted in inserting a tube into the trachea of a fresh corpse and performing multiple posturing techniques such as lifting the arms and pressing on the back or chest, lifting the hips, and rocking the deceased patient. He then observed the effects of these procedures via a respirometer connected to the tracheal tube. His results were first published in the Journal of the American Medical Association in 1950 (2).

In 1951, Gordon performed similar studies on medical students anesthetized with curare. Later that year he published a wealth of data (3) supporting the notion that these techniques were able to provide some degree of manual respiration. There were two limitations to Gordon’s relentless efforts. The first was that he only alluded to the idea of mouth-to-mouth ventilation and did not evaluate this technique, and the second was that all of his data were collected in intubated patients in whom the airway was fully protected.

Simultaneous with these efforts, James Elam discovered that by merely using expired air one could oxygenate humans adequately. His discovery was born of a need to ventilate patients suffering from acute paralysis during a polio epidemic in 1946. His repeated experience in performing mouth-to-nose breathing over a period of several years convinced him of its value. To document his beliefs scientifically, in 1954 Elam studied intubated, anesthetized, nonbreathing postoperative patients. He merely blew into their tracheal tubes with his own exhaled air and documented that by doing this he could maintain normal arterial oxygen saturation.

It was not until 1956 that fate brought Elam and his data together with Peter Safar. Lively discussion enticed Safar to begin experiments on mouth-to-mouth artificial respiration. By 1957, Safar had proven that the mouth-to-mouth technique was clearly superior to the manual ventilation techniques that were currently employed and that it could be performed quite easily by laypersons (4). He was also able to document that tilting a person’s head backward usually maintained the airway open, thus supporting previous data from patients with protected airways. By 1958, the work of Gordon, Elam, and Safar persuaded the American Medical Association and the U.S. Military to adopt the mouth-to-mouth technique as the official means of providing artificial respiration.

Use of electrotherapy was a common practice for a variety of ailments ranging from paresis to death throughout much of the eighteenth and nineteenth centuries. Unfortunately, little was known about electrical forces or the ailments it purportedly treated, and there was no benefit to survival from its use. In fact, it took several decades to link electricity to the appropriate treatment for many causes of sudden death. Until the development of the electrocardiograph, ventricular fibrillation was a diagnosis that could only be made by observing the heart. It was first described in 1850 by Karl Ludwig in the dog lab (5). Ludwig noted that he could induce ventricular fibrillation by applying galvanic currents directly to a dog’s heart. Although this was likely the first link between electricity and sudden death, the connection was ignored for decades. In 1889, John McWilliam refuted the notion that sudden cardiac death was caused by ventricular standstill by describing a fibrillating heart in the dog lab. He documented, as others had before him, that electricity could induce this event in the canine model (6). Unfortunately, he never attempted to use electricity to terminate the events. Although he postulated that a similar scenario might occur in humans, he did not pursue this. It was not until a decade later that two French physiologists, Frederic Battelli and Jean Louis Prevost, reported that, although a weak current passed through the heart could cause fibrillation, a stronger current was capable of terminating it (7). This singularly important discovery remained dormant for the next several decades.

In the late 1920s the Electric Company and Edison Power Company reconsidered the idea of coupling electricity with defibrillation. They commissioned William Kouwenhoven, Donald Hooker, and Orthello Langworthy at the Johns Hopkins University to research electrical effects on the heart. This group quickly documented that weak shocks could induce ventricular fibrillation and stronger shocks could eradicate it. They were the first to discover that defibrillation could be successfully performed without opening the chest (8). The group also coined the term “countershock,” which was used synonymously with defibrillation. An initial shock placed the heart into ventricular fibrillation and a subsequent countershock could terminate it. None of these researchers pursued the possibility of using this countershock in humans to terminate ventricular fibrillation.

Two decades passed until Claude Beck successfully defibrillated a patient. Based on the work of Kouwenhoven, Hooker, and Langworthy, Beck constructed an alternating current (AC) internal defibrillator. Although he was successful in resuscitating a pediatric patient who had developed ventricular fibrillation during cardiac surgery, it took another 8 years for him to successfully use his device on another patient.

In 1955, Paul Zoll developed an external alternating current defibrillator. On a case- by-case basis, he documented that external defibrillation could be performed safely and effectively (9).

Defibrillators utilizing alternating current were quite heavy and cumbersome. It was very difficult to transport this equipment to needy patients in an emergency situation. In 1960, Bernard Lown developed a direct current (DC) defibrillator that was battery operated and readily transportable. This piece of equipment was the first in a long line of modern direct current defibrillators.

The first documented case of closed-chest compression for the treatment of cardiac arrest in the United States was in 1904 (10). Without the aid of defibrillation or pacing to restart the heart the concept was not particularly useful, and it never gained extensive popularity. It was not until the late 1950s that the technique of closed-chest massage was rediscovered. William Kouwenhoven and Guy Knickerbocker were studying fibrillation in their animal laboratory at the Johns Hopkins University. While performing experiments to determine how long a canine’s heart could be left fibrillating and still be successfully cardioverted, Knickerbocker noted that when he placed the defibrillator paddles snugly against the closed chest of the dog there was a slight increase in arterial pressure. The investigators noted that by applying the paddles in a repetitive motion they could prolong the time that the heart could stay in fibrillation and be defibrillated successfully. James Jude joined the group, and the team began performing multiple studies using the hands to compress the chest. Through a series of trial and error experiments, it was determined that applying a downward pressure of 1 1/2 to 2 inches on the lower sternum at a rate of 60 to 80 per minute was the optimal way to perform this maneuver. The investigators published data derived from patients suffering from in-hospital cardiac arrest in 1960. Fourteen of 20 patients survived to discharge from the hospital (11). It was finally understood that closed-chest compressions could “buy time” for the patient with a fibrillating heart until an external defibrillator arrived.

It was not until Safar, Kouwenhoven, and Knickerbocker presented their scientific data at the Maryland Medical Society meeting on September 16, 1960, that artificial ventilation was combined with artificial circulation to create CPR. The trio lectured around the world to promote the concept of CPR. Gordon produced a training film in 1962 and coined the mnemonic ABC for airway, breathing, circulation. The popularity of this technique, which could be performed by anyone and anywhere, spread quickly.

The American Heart Association officially endorsed CPR in 1963 and developed a CPR Committee. In 1966 the National Research Council of the National Academy of Sciences brought together representatives from more than 30 organizations, including the American Red Cross, and established official recommendations regarding standardized training and performance of CPR (12). Since then, the American Heart Association has hosted special conferences in 1973, 1979, 1985, 1992, 2000, and 2005 to establish consensus recommendations for resuscitation. Each of these conferences was followed by publication of educational documents that have been used worldwide to teach the science of resuscitation.

For 15 years after the discovery of closed-chest compression, it was generally believed that blood flow during CPR is caused by direct compression of the heart between the sternum and the spine (“cardiac pump” theory). In the 1970s, the “cardiac pump” theory was challenged by investigators who observed that increased intrathoracic pressure alone (without precordial compression) can generate blood flow. Criley et al. (13) reported that increases in intrathoracic pressure by repeated coughing could maintain adequate systemic blood pressure and flow to maintain consciousness without precordial compression in a patient who developed ventricular fibrillation during cardiac catheterization. This observation was confirmed by Niemann et al. (14), lending further support to the notion that pressurization of the thoracic cavity could generate blood flow and pressure by forcing blood out of both the heart and thoracic vessels. Sudden increase in the intrathoracic pressure causes air trapping in the alveoli and small bronchioles during chest compression, creating a pressure gradient between the intrathoracic and extrathoracic cavities (15). According to this “thoracic pump” theory, the heart functions as a passive conduit (16). Pressurization of the thorax collapses veins at the thoracic inlet, preventing venous backflow (17). Forward flow occurs because the more muscular arteries remain open, particularly if epinephrine is administered exogenously.

The relative contributions of the cardiac and thoracic pump mechanisms have been debated (16,18,19,20). Transesophageal echocardiography studies during cardiopulmonary resuscitation demonstrate that both mechanisms are operative in humans (19,21,22,23,24). Sternal compression virtually always squeezes blood out of the right ventricle (cardiac pump), whereas the amount of left ventricular compression is highly variable among patients (22). Physiologic studies in experimental models (25) and humans (26) suggest a strong role for the thoracic pump. In addition, active decompression of the chest by application of negative pressure or suction to the sternum can further enhance cardiac output by improving venous inflow (27,28,29,30,31,32). Finally, interposing an abdominal compression between each pair of chest compressions has also been tried in an attempt to mimic the physiologic effects of intraaortic balloon counterpulsation (27,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55).

Weisfeldt and Becker postulated that there are three physiologic phases of resuscitation: electrical, circulatory, and metabolic (56). When cardiac arrest occurs due to ventricular fibrillation, myocardial cells are rich in adenosine triphosphate (ATP) for the first 3 to 4 minutes (electrical phase). During the first few minutes, prompt defibrillation may be all that is required to restore the circulation. However, fibrillating myocardial cells consume ATP at a nearly normal rate (57). After several minutes, myocardial ATP stores are reduced sufficiently so that a defibrillation shock will ablate the ventricular fibrillation but will usually result in either asystole or pulseless electrical activity (PEA). During this “circulatory phase,” a brief (90 seconds to 3 minutes) period of effective CPR before defibrillation will boost myocardial ATP stores and increase the likelihood that a perfusing rhythm will result (58). This “CPR-first” strategy is now being used increasingly for patients whose cardiac arrest was not witnessed by trained health-care providers (59,60). The standard “shock-first” strategy is still advisable when a patient is witnessed to go into ventricular fibrillation and defibrillation can be accomplished within the first 3 to 4 minutes. If the patient remains in cardiac arrest from more than approximately 8 minutes, increasing ischemic cellular injury occurs that currently cannot be corrected with chest defibrillation and conventional CPR alone. This period is termed the “metabolic phase” of resuscitation, indicating that cellular-protective measures will likely be needed for successful recovery of vital organ function.

Minimal interruption of chest compression during resuscitation is important to maximize tissue oxygen delivery and, hence, myocardial ATP reserves. Unfortunately, chest
compressions are not maintained for as much as 40% to 50% of the time during a typical resuscitation, particularly if automated external defibrillators (AEDs) are used (61). The odds of success increase when continuous, or nearly continuous, chest compressions are performed during resuscitation (62). Shortening the time interval from the last chest compression until a defibrillation shock is administered (“hands-off interval”) can also increase the likelihood that a defibrillation shock will result in return of spontaneous circulation (ROSC) (63,64). It is important to ensure that complete chest wall decompression occurs during the upstroke on the sternum to improve venous filling (65). Finally, recent evidence suggests that hyperventilation may be harmful during resuscitation because it increases intrathoracic pressure, causing a marked decrease in venous filling. This paradoxically reduces cardiac output and tissue oxygen delivery (66,67).

Survival from pulseless ventricular tachycardia or ventricular fibrillation is inversely related to the time interval between its onset and termination. Each minute that a patient remains in ventricular fibrillation, the odds of survival decrease by 7% to 10% (90). Survival is highest when CPR is started within the first 4 minutes of arrest and advanced cardiac life support (ACLS), including defibrillation and drug therapy, is started within the first 8 minutes (91). The American Heart Association’s Emergency Cardiovascular Care Committee and its Advanced Cardiovascular Life Support Subcommittee began to widely publicize the “chain of survival” concept in 1991. This phrase represents a sequence of events that should occur in most cardiac arrest cases to maximize the odds of successful resuscitation (90). The steps include early recognition of the problem and activation of the EMS system by a bystander, early CPR, rapid provision of defibrillation for patients who need it, and advanced cardiac life support (e.g., intubation, administration of medications). Schematically, this sequence can be depicted as a “chain of survival” (Fig. 69.1).

The American Heart Association’s Advanced Cardiac Life Support (ACLS) algorithms provide a framework for dealing with life-threatening cardiopulmonary emergencies in a logical sequence (101,102). There are sections of the algorithm for initiating CPR and for treating patients with ventricular fibrillation or pulseless ventricular tachycardia, bradycardia, asystole, and pulseless electrical activity (PEA), which was formerly known as electromechanical dissociation (EMD). However, the algorithms are not appropriate for every clinical circumstance, and the team leader must adapt them and the general ACLS principles when necessary. Resuscitation team leaders are encouraged to function as “thinking cooks” when applying these cookbook procedures.

Maintenance of both the systolic and diastolic arterial pressure is vital during CPR. Because flow to most vital organs (except the heart) occurs during systole, a minimal systolic arterial pressure of 50 to 60 mm Hg is usually required to resist arteriolar collapse (133). Diastolic pressure is also important because it is a critical determinant of the coronary perfusion pressure (CPP = aortic diastolic – right atrial pressure) during CPR. CPP is one of the best hemodynamic predictors of ROSC in both animal models (20,134,135,136,137,138,139,140,141,142,143,144) and humans (145). A minimal threshold gradient for CPP of approximately 15 mm Hg (usually corresponding to an aortic diastolic pressure of 30 to 40 mm Hg) provides a level of myocardial blood flow that is necessary to meet the metabolic needs of the arrested myocardium (146) and to achieve ROSC (145).

A cuff manometer can be used to estimate the systolic arterial pressure during CPR by palpating the brachial artery or listening over it for flow with a peripheral Doppler device
(147). More accurate, invasive measurements of systolic and diastolic pressure can be obtained by inserting an arterial line into the radial, brachial, or femoral artery (26,148,149,150,151,152,153,154,155). Table 69.1 summarizes recent published invasive arterial pressure measurements during resuscitation in adult humans. Conventional CPR generates systolic, diastolic, and coronary perfusion pressures that are inadequate to sustain blood flow and function in vital organs (e.g., the brain). These measurements explain why cardiac arrest patients are rarely conscious during CPR.

Generation of a satisfactory arterial pressure is a prerequisite for adequate flow to vital organs; however, the presence of a reasonable arterial pressure does not ensure that there will be sufficient flow to meet metabolic needs. Pulmonary artery catheters are inserted infrequently during resuscitation because they are time consuming to set up and technically difficult to position. The low flows generated by CPR do not favor ready passage of the balloon-flotation catheter through the right heart. In addition, it is difficult to determine the catheter tip’s position from pressure recordings because the pressures in the intracardiac chambers and great vessels are similar to each other during closed-chest CPR (25,156,157,158,159,160). Fluoroscopy is of little value during CPR, even if it is available, because it is not easy to continue chest compression impeded by the machine’s C-arm. Transesophageal echocardiography (TEE) offers the greatest promise as a means of visualizing and helping to position intracardiac catheters successfully during CPR.

Despite these technical limitations, there have been several published reports of intracardiac pressure and flow measurements in humans who were already being monitored invasively in an intensive care unit at the time of their cardiac arrest (161,162,163,164). Conventional, closed-chest CPR in adult humans produces a hemodynamic state resembling profound cardiogenic shock, with a low systemic arterial pressure, markedly reduced cardiac output, and high intravascular filling pressures. Hemodynamic monitoring post-CPR may be useful for managing selected patients who survive resuscitation, but the risks, potential benefits, and cost implications must be weighed on a case-by-case basis (164).

The percentage of carbon dioxide contained in the last few milliliters of gas exhaled from the lungs with each breath is known as the end-tidal carbon dioxide concentration (P_etCO₂) (165,166). It can be measured by passing an infrared beam through exhaled gases and measuring the decrease in voltage output from a photoelectric cell calibrated to the wavelength at which carbon dioxide absorbs light. It can also be estimated by attaching an inexpensive disposable plastic, colorimetric device in-line between the endotracheal (ET) tube and the ventilation device. Color indicators on the device change hue as the exhaled gases pass through the monitor’s pH-sensitive membranes. The membrane’s color can be compared with the adjacent color chart on the device, thus indicating the percentage P_etCO₂.

Two important terms need to be defined with respect to end-tidal carbon dioxide monitoring. Capnography refers to any technology that displays and/or prints the actual capnographic waveform. If an unmistakable capnographic waveform is detected when a capnographic probe is attached to a patient who is being ventilated, then the airway device is unequivocally ventilating the lungs. Capnometry refers to the measurement or estimation of the end-tidal carbon dioxide concentration. It can be displayed in analogue or digital format, or it can be approximated using a colorimetric detection device. Capnometry often provides useful information on the anatomic location of an airway device (e.g., ET tube); however, it does not provide the degree of definitive certainty that the presence of a capnographic waveform does.

During normal respiration and circulation, the P_etCO₂ averages 4% to 5%. Two units of measure are popularly used in reporting the P_etCO₂: percent and mm Hg (1% is approximately 7 mm Hg). There is a logarithmic relationship between the P_etCO₂ and the cardiac output (167). At normal or elevated levels of cardiac output, ventilation is the rate-limiting factor responsible for eliminating the large amount of carbon dioxide traversing the pulmonary circuit (e.g., hyperventilation lowers, and hypoventilation raises, the P_etCO₂). In this range, if blood flow and arterial pressure are kept reasonably constant, the P_etCO₂ closely approximates arterial carbon dioxide tension (P_aCO₂) and can be used as a “real-time” guide to the
adequacy of ventilation (the P_etCO₂ actually lags behind real-time events by a few seconds, the amount of time it takes for exhaled gas to be drawn into the machine and analyzed) (168).

The P_etCO₂ can also be used to confirm ET airway placement, particularly in the non–cardiac arrest patient who has a pulse and an adequate blood pressure (where the sensitivity and specificity of the P_etCO₂ for detecting correct ET tube placement approach 100% and 90%, respectively) (154,169,170,171,172,173). The ET tube cuff should be inflated when the P_etCO₂-monitoring device is attached to ensure that the gas being sampled is from the structure (i.e., trachea or esophagus) in which the tube resides. Ventilation through an ET tube that has been properly inserted in the trachea yields a P_etCO₂ of 4% to 5% in a patient with a normal cardiac output and no significant ventilation/perfusion gradient; ventilation through an ET tube that has been inadvertently inserted into the esophagus results in a P_etCO₂ of less than 0.5%. The only important exception occurs when the ET tube is inserted into the esophagus of a patient who has recently ingested a carbonated beverage (e.g., beer, soda pop). In such a case, the initial P_etCO₂ will appear to be normal or high on the first few ventilations but will typically decrease rapidly to less than 0.5% by the sixth or seventh ventilation (174).

At low levels of cardiac output (below approximately 50% of normal in animal models), ventilation has much less effect on the P_etCO₂. Instead, the pulmonary blood flow (and the subsequent ventilation/perfusion mismatch) is the rate-limiting factor determining the P_etCO₂. If ventilation is kept relatively constant in this range, an increase or a decrease in the cardiac output will usually be reflected by a rise or fall in the P_etCO₂, respectively.

During CPR the cardiac output falls typically to between one fourth and one third of normal (162,175,176,177). The P_etCO₂ also decreases to between one fourth and one third of normal as the reduced cardiac output and pulmonary blood flow present less blood and carbon dioxide to the lung for exchange with oxygen in the pulmonary capillary (178

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