Review Article

Current Concepts

Jane F. Desforges, M.D., Editor

Cardiopulmonary Resuscitation

James T. Niemann, M.D.

N Engl J Med 1992; 327:1075-1080October 8, 1992DOI: 10.1056/NEJM199210083271507

Article

CARDIOPULMONARY arrest can be defined as the abrupt cessation of spontaneous and effective ventilation and systemic perfusion (circulation). Cardiopulmonary resuscitation (CPR) provides artificial ventilation and circulation until advanced cardiac life support can be provided and spontaneous cardiopulmonary function restored. Patients most likely to benefit from CPR (i.e., to be successfully resuscitated) include the following: those with witnessed sudden arrest due to ventricular fibrillation outside the hospital, when electrical countershock can be performed within approximately seven to eight minutes; hospitalized patients with primary ventricular fibrillation and ischemic heart disease; those with cardiac arrest in the absence of life-threatening coexisting conditions; and those with hypothermia, drug overdose, airway obstruction, or primary respiratory arrest.1 ^, 2

Causes of Cardiopulmonary Arrest

Cardiopulmonary arrest is usually the result of a cardiac arrhythmia. Sudden cardiac death outside the hospital is most often caused by ventricular fibrillation in patients with multivessel atherosclerotic coronary artery disease. When ventricular fibrillation occurs outside the hospital, it is usually presumed to reflect chronic myocardial ischemia with electrical instability, rather than acute myocardial infarction.3 In contrast, arrest in the hospital most often follows acute myocardial infarction or is the result of severe multi-system disease, and asystole, a bradyarrhythmia, or electromechanical dissociation is the commonly encountered rhythm, often after a period of protracted hypotension.2 ^, 4 5 6 The rates of survival to hospital discharge after cardiopulmonary arrest and resuscitation in and outside the hospital are similar and generally range from 10 to 20 percent, although higher and lower rates have been reported.7

Diagnosis of Cardiopulmonary Arrest

In cardiopulmonary arrest, the cessation of cardiopulmonary function is followed almost immediately by the cessation of cerebral function. The patient becomes unresponsive to sensory stimulation, and brief, generalized seizure activity typically occurs after about 15 seconds of complete cerebral anoxia. The absence of ventilation can be determined by assessing chest expansion visually, by auscultation, or by feeling for the movement of air from the mouth or nostrils. The presence of a pulse should be assessed by palpation of the carotid or femoral artery. The absence of a palpable pulse and the presence of unresponsiveness and apnea confirm the diagnosis of cardiopulmonary arrest. The diagnosis should be well established because CPR, even when properly performed, is associated with a number of complications that may affect care and survival.8

Management of Cardiopulmonary Arrest

The initial management of cardiopulmonary arrest will vary depending on the availability of equipment to monitor cardiac rhythm and perform countershock. In the hospital, such equipment should be available within minutes. If ventricular fibrillation or ventricular tachycardia is the first rhythm documented by conventional monitoring or with "quick look" defibrillation paddles, three sequential countershocks should be delivered as soon as possible at energy settings of 200, 200 to 300, and then 360 J.9 If ventricular fibrillation is not the initially recognized rhythm or if countershock is not successful in establishing an effective rhythm, chest compressions and artificial ventilation should be initiated. If the arrest occurs outside the hospital, the rescuer should immediately summon assistance (i.e., in the United States, dial 911) and then begin CPR while waiting.

Artificial Circulation and Chest Compressions

In 1960, Kouwenhoven et al. reported that rhythmic depression of the sternum in animals produced pulsations in arterial pressure and permitted successful closed-chest electrical defibrillation after prolonged ventricular fibrillation.10 It was assumed that anterior-to-posterior sternal depression selectively compressed the cardiac ventricles between the sternum and vertebrae, thereby creating an artificial systole with increases in intraventricular pressure, atrioventricular valve closure, and forward right- and left-heart outflow during compression. During the relaxation phase (CPR diastole), right- and left-heart passive filling was presumed to occur. This method of artificial circulation during cardiac arrest was rapidly adopted, since it was easily performed without thoracotomy and manual cardiac massage. Closed-chest compressions in humans were later shown to produce only a limited cardiac output (<30 percent of normal) that is unlikely to sustain vital-organ perfusion and viability.11

A number of observations have provided evidence about possible physiologic mechanisms for blood flow during chest compression and have defined the determinants of cerebral and myocardial perfusion. Forceful spontaneous coughing by patients during ventricular fibrillation in a monitored setting and electrically induced coughing in an animal model of cardiac arrest suggest that blood flow during CPR may result solely from phasic fluctuations in intrathoracic pressure.12 ^, 13 This hypothesis is supported by the results of hemodynamic and angiographic studies in animal models and by the results of hemodynamic and echocardiographic studies in humans.14 15 16 17 18 These studies demonstrate that blood flow during sternal depression is not dependent on ventricular compression. Chest compression causes a generalized and nonselective increase in intrathoracic intravascular pressures that are differentially transmitted to the peripheral circulation because of the closure of venous valves, the result of an abrupt and rapid increase in intrathoracic venous pressure during chest compression.15 ^, 19 ^, 20 This concept of the mechanism of blood flow, generally referred to as the thoracic pump, is also supported by computer models of circulatory arrest and CPR.21 ^, 22

Recent studies have also defined critical arteriovenous pressure gradients that determine the perfusion of vital organs during CPR. Jugular venous valve closure in the brachiocephalic circulation establishes a perfusion gradient across the cerebral circulatory bed during sternal depression.15 ^, 19 ^, 20 The difference between aortic and right atrial pressure between rhythmic chest compressions (CPR diastole) is the principal determinant of myocardial perfusion during cardiac arrest and CPR.23 This latter gradient is also the principal determinant of successful cardiac resuscitation — i.e., the restoration of a spontaneous perfusing cardiac rhythm.24 25 26 Even with "adequate" chest compressions, however, cerebral blood flow in animal models is typically less than 30 percent of prearrest values, and myocardial blood flow is less than 10 percent.23

Other studies provide some support for the traditional concept that cardiac compression has a role in providing systemic perfusion.27 28 29 Right ventricular compression, or left ventricular compression during late sternal depression, may contribute to cardiac output. Regardless of the mechanism of blood flow, the pressure gradients for the perfusion of vital organs and successful resuscitation are the same. It is probable that the pressure gradients for blood flow during CPR are interactive. The predominant mechanism and physiology may depend on heart size, the anterior-posterior dimensions of the chest, thoracic compliance, the force and depth of sternal depression, and the ratio of chest compression to relaxation.30

In animal models, optimal cardiac output and perfusion during closed-chest CPR appear to depend on both the rate of chest compression and the ratio of CPR time in systole to time in diastole. A chest-compression rate of 80 to 100 compressions per minute is currently recommended at a force that produces 1.5 to 2 inches (3.8 to 5 cm) of anteroposterior sternal displacement in adults. At this rate, the optimal ratio of CPR systolic to diastolic time (1:1) is most likely to be achieved.30

Artificial Ventilation

Endotracheal intubation is the optimal method of airway management and artificial ventilation during cardiopulmonary arrest. Other methods have been described (esophageal-obturator and multiluminal airway devices).31 ^, 32 However, multiluminal devices are blindly inserted into the upper airway, their ventilatory effectiveness dependent on a tight seal between face and mask, and they have frequently been associated with complications or inadequate ventilation.33 Mouth-to-mouth or mouth-to-mask ventilations at a volume of 0.8 to 1.2 liters per breath delivered over a period of 1.5 to 2 seconds are preferred when endotracheal intubation cannot be performed.

After endotracheal intubation, artificial ventilation should be performed at a rate of one ventilation to five chest compressions, with either a bag-valve device or a mechanical ventilator. If the airway is secured, ventilations can be interposed between compressions or performed during chest compression. Simultaneous chest compression and airway ventilation improve cerebral perfusion in animal models of arrest and resuscitation.19 ^, 20 When the airway is not protected, ventilations should be administered between chest compressions. Effective artificial ventilation is a primary intervention that reduces hypercapnia and arterial acidemia during resuscitation.

Advanced Cardiac Life Support

As stated previously, if ventricular fibrillation is the first rhythm encountered, sequential attempts at electrical defibrillation should be performed. If ventricular fibrillation is not the first rhythm encountered, or if countershock results in persistent ventricular fibrillation or another nonperfusing spontaneous cardiac rhythm, endotracheal intubation should be performed, chest compressions initiated, and an intravenous line established. Subsequent management depends on the observed rhythm.

Ventricular Fibrillation

The cardiac response to countershock is largely time-dependent. If countershock can be performed within three minutes of the onset of ventricular fibrillation, 70 to 80 percent of patients will convert to a rhythm associated with adequate perfusion.34 If countershock is attempted later, the success rate rapidly declines. Although ventricular fibrillation may be terminated, the chance of a return of effective cardiac function is smaller.34 ^, 35 After five minutes of ventricular fibrillation, countershock rarely results in a spontaneous perfusing rhythm; asystole, electromechanical dissociation, or persistent ventricular fibrillation are the usual results.36

If countershock fails to end ventricular fibrillation, or if a perfusing rhythm fails to follow countershock, 1 mg of epinephrine should be administered intravenously. The beneficial effects of epinephrine depend primarily on its alpha₁-adrenergic effects, which include arterial vasoconstriction and selective redistribution of cardiac output.37 Epinephrine increases the CPR diastolic aortic-to-right-atrial myocardial perfusion gradient by increasing aortic pressure and improves the cerebral perfusion gradient by increasing carotid arterial pressure. Its effects on myocardial perfusion largely explain its benefits on the outcome of resuscitation in laboratory models.

It remains unclear whether antiarrhythmic agents (lidocaine and bretylium) are of value if repeated countershocks and epinephrine fail to terminate persistent or refractory ventricular fibrillation. In any case, there are no data to support the use of one drug over the other.38

Asystole

Asystole is commonly the first documented rhythm in victims of unwitnessed sudden cardiac arrest outside the hospital and in critically ill inpatients. This initially encountered rhythm is nearly always fatal (rate of survival to hospital discharge, <2 percent). Currently recommended therapy includes intravenous epinephrine (1.0 mg) and atropine (0.5 to 1.0 mg).

The value of immediate artificial cardiac pacing with new, noninvasive (transcutaneous) methods is unproved in the typical asystolic arrest, as is the use of percutaneous (needle) transthoracic pacing.39 ^, 40 Asystole after electrical defibrillation of prolonged ventricular fibrillation is common and is usually a fatal outcome of countershock.41 If countershock of ventricular fibrillation of short duration is followed by asystole, effective CPR and pharmacologic support with epinephrine may be of value.

A single study in animals suggests that ventricular fibrillation has an electrical force vector and may masquerade as asystole if only a single electrocardiographic lead is monitored. This conclusion, however, was based on the monitoring of leads rarely used in humans (precordial and augmented limb leads).42 There are clinical data to suggest that the phenomenon is rare.43

Nonperfusing Rhythm

A cardiac rhythm without arterial pulsations is generally referred to as electromechanical dissociation and can be due to a number of causes (e.g., cardiac tamponade, tension pneumothorax, and hypovolemia). In the setting of cardiac arrest, the definition of electromechanical dissociation is not uniform. Electromechanical dissociation with wide QRS complexes at a slow rate (a pulseless idioventricular rhythm) is likely to have a different cause than electromechanical dissociation with rapid, narrow QRS complexes.44 When electromechanical dissociation is the initially encountered rhythm or when it follows countershock for ventricular fibrillation, recommended interventions include artificial ventilation and circulation or epinephrine (1 mg intravenously) and atropine (1 mg intravenously). There are no data to suggest that needle thoracostomy, pericardiocentesis, or intravenous volume infusion should be routinely performed in a patient with nontraumatic cardiac arrest when electrocardiographic QRS complexes are wide, slow, and not associated with palpable pulses.

Monitoring the Effectiveness of CPR

The palpation of a peripheral pulse during CPR should not be relied on to assess the adequacy of systemic perfusion. Arterial blood gas measurements are also of no value in assessing systemic perfusion. An arteriovenous blood gas "paradox" has been described in both animal models and humans during cardiac arrest and CPR.45 ^, 46 Arterial blood samples typically reveal a high oxygen saturation, a low partial pressure of carbon dioxide, and a progressive metabolic acidosis. Venous samples, however, demonstrate a marked difference between arterial and venous oxygen, hypercarbia, and a wide arteriovenous difference in pH. These differences are due to the limited systemic perfusion provided by closed-chest CPR and the resulting metabolic products of anaerobic metabolism.

A number of studies in animals and humans suggest that systemic perfusion during arrest and CPR is related to the end-tidal volume of carbon dioxide, which is an indirect measure of pulmonary perfusion.47 The end-tidal volume of carbon dioxide has been shown to correlate directly with cardiac output and myocardial perfusion pressure during CPR. End-tidal carbon dioxide measurements can be performed noninvasively in the acute care setting. An increasing end-tidal carbon dioxide value may be the first indication of the restoration of spontaneous circulation and may be predictive of successful resuscitation.

Controversies and Recent Observations

Alpha-Adrenergic Drug Therapy

The value of alpha-adrenergic drugs (epinephrine, norepinephrine, phenylephrine, and methoxamine) is well supported in studies in animals.48 These agents selectively increase arterial pressure and the defined pressure gradients for cerebral and myocardial blood flow during cardiac arrest and CPR. The hemodynamic effects appear to be dose-dependent. In laboratory investigations and limited studies in humans, no alpha-adrenergic agonist has been shown to be superior to epinephrine. The beneficial hemodynamic effects of epinephrine on cerebral and myocardial perfusion during CPR in animal models are clearly dependent on the dose (in milligrams per kilogram of body weight).37 The currently recommended dose of epinephrine, which is approximately 0.01 mg per kilogram, may not be hemodynamically optimal. Higher doses of epinephrine (0.1 to 0.2 mg per kilogram) improve cerebral and myocardial perfusion and the outcome of resuscitation efforts in studies in animals. However, a large, multicenter trial showed that high-dose intravenous epinephrine (0.2 mg per kilogram) administered by paramedics had no advantage over standard-dose intravenous epinephrine (0.02 mg per kilogram) in patients who had cardiac arrest outside the hospital.49 Furthermore, a high dose of epinephrine (7 mg), as compared with a standard dose (1 mg), administered in the emergency department or to inpatients did not improve survival or neurologic outcome.50

Acid–Base Balance and Buffer Therapy

Sodium bicarbonate is commonly used to treat metabolic acidosis regardless of its cause, and before 1986 it was used early and frequently during cardiac arrest and prolonged resuscitation efforts. Acidemia has been shown to decrease myocardial contractility and attenuate the hemodynamic response produced by catecholamines.51 Because of this, treating metabolic acidosis should theoretically improve the outcome of resuscitation efforts. Early work suggested that the administration of sodium bicarbonate and epinephrine after 10 minutes of ventricular fibrillation followed by 4 to 10 minutes of CPR and countershock improved the chances of resuscitation and long-term survival when compared with the use of epinephrine alone or placebo.52 When sodium bicarbonate was used alone, however, the outcome was no different from that in the control group. It should be noted that arterial pH was not measured in this study during arrest and resuscitation. A later study in an animal model of three minutes of ventricular fibrillation followed by three minutes of open-chest cardiac massage and then countershock demonstrated that tromethamine and sodium bicarbonate did not improve the success of defibrillation when compared with a normal saline control.53 However, arterial pH ranged from 7.32 to 7.39 immediately before the administration of the drug or placebo. Lower values are more likely in the more common clinical setting of prolonged arrest and CPR.

Recent work in clinically relevant animal models has failed to show that buffer agents improve outcome. Administering buffer agents that generate carbon dioxide may in fact be detrimental.54 55 56 When sodium bicarbonate reacts with hydrogen ions, carbon dioxide is liberated. If ventilation is insufficient to eliminate the carbon dioxide, it will accumulate, rapidly penetrate cell membranes, and worsen intracellular acidosis. The 7.5 percent preparation of sodium bicarbonate that is currently used is hypertonic, and hypertonic solutions decrease aortic pressure during CPR, thus decreasing the myocardial perfusion gradient, the major determinant of successful cardiac resuscitation. Carbicarb, an equimolar mixture of sodium bicarbonate and sodium carbonate and a buffering agent that does not generate carbon dioxide, has been studied during cardiac arrest and CPR. It does not improve resuscitation outcome during prolonged arrest and CPR. It is also hypertonic and decreases the CPR myocardial perfusion pressure.

Severe metabolic acidosis develops late during resuscitation efforts, typically after about 20 minutes of arrest and CPR if artificial ventilation causes hypocapnia. Initial resuscitation efforts should be directed toward prompt countershock of ventricular fibrillation, effective chest compression, hyperventilation, and the use of epinephrine to increase the myocardial and cerebral perfusion gradients. The early or late use of buffering agents is of no proved value.

Calcium Chloride

Although the value of calcium for cardiac arrest had never been proved, calcium therapy was commonly used for asystole and electromechanical dissociation until 1986.57 During the 1980s the role of intracellular calcium uptake during prolonged cellular ischemia and in the genesis of irreversible cellular injury was described and debated.58 Because of the potential role of intracellular calcium accumulation in irreversible ischemic cell injury, calcium is now recommended only in selected situations (e.g., hyperkalemia, calcium-channel—blocker toxicity, and hypocalcemia).

Recent clinical studies indicate that levels of ionized calcium decrease during prolonged cardiac arrest and CPR,59 ^, 60 but the mechanism for this change and its influence on the outcome of resuscitation efforts remain unclear.

Site of Drug Administration

Intravenous drug administration is preferred during advanced cardiac life support. There are no conclusive data to support the use of a central venous rather than a peripheral venous route. Although a number of drugs commonly used during advanced cardiac life support (epinephrine, atropine, and lidocaine) may be systemically absorbed after endotracheal administration and transalveolar uptake in animals with spontaneous perfusion, there are no data to support this route at currently recommended doses in the setting of cardiac arrest and resuscitation.61 Substantially higher doses of endotracheally administered drugs are required to produce the effect of smaller intravenous doses. Intraosseous administration has been shown to be an effective alternative in children,62 but it has not been studied in adults.

End-Tidal Carbon Dioxide

In uncontrolled clinical studies, the mean end-tidal volume of carbon dioxide predicts the results of cardiac-resuscitation efforts but not hospital survival.63 ^, 64 Although promising as a noninvasive monitoring method, end-tidal carbon dioxide measurements are affected by therapeutic interventions. Epinephrine increases myocardial and cerebral perfusion during CPR, but total cardiac output decreases as flow is redistributed, pulmonary blood flow decreases, and end-tidal carbon dioxide decreases.65 The administration of sodium bicarbonate increases the partial pressure of venous carbon dioxide and will increase endtidal carbon dioxide, through its buffer effects and generation of carbon dioxide, regardless of the volume of pulmonary blood flow. At present, end-tidal carbon dioxide determinations should neither dictate therapeutic interventions nor serve as an indicator of when to continue or terminate CPR.

Open-Chest CPR

Although a number of experimental studies in animals and a single clinical study clearly indicate that open-chest direct cardiac compression produces greater cardiac output and higher critical perfusion gradients than does closed-chest CPR,11 ^, 66 ^, 67 studies in animals and humans indicate that open-chest CPR is of no value after prolonged closed-chest CPR.68 69 70 Open-chest CPR should be restricted to the operating room and selected instances of penetrating thoracic injury.

When to Start and When to Stop CPR

The decision to initiate, withhold, or forgo CPR has presented substantial medical and ethical problems for health care professionals, patients, and the families of patients. One of the major issues, patient autonomy, has been addressed at the national level with the introduction of do-not-resuscitate protocols, the report of the President's Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research, and most recently, the enactment of the Patient Self-Determination Act of 1990. These actions have encouraged discussion between physicians, patients, and families regarding the use of medical interventions or therapies, including CPR. One issue that has not been resolved is whether a physician is obliged to initiate CPR at the wish of the patient or his or her representative or surrogate when the physician believes that CPR will not prolong life.71 ^, 72 Studies of in-hospital cardiac arrest and the outcome of CPR have demonstrated that certain groups of patients do not survive.2 ^, 4 ^, 5 Such patients include those with oliguria, metastatic cancer, sepsis, pneumonia, and acute stroke.

Do-not-resuscitate protocols for cardiac arrest outside the hospital have been or are being established in several states to allow rescuers to forgo attempts to resuscitate the terminally ill. When to cease resuscitation attempts once they have been started is currently being addressed.73 ^, 74 Available data indicate that victims of cardiac arrest outside the hospital do not benefit from continued resuscitation efforts in the hospital after optimal prehospital efforts have failed. Of 1445 patients in eight studies, only 10 (0.7 percent) survived to be discharged from the hospital.73 Six of the 10 had a second cardiac arrest after initial resuscitation.

After more than 30 years of widespread use of CPR, a reevaluation of its benefits in terms of survival and quality of life shows it to be a desperate effort that will help only a limited number of patients. For most, CPR is unsuccessful. Although potentially lifesaving, it will continue to present ethical dilemmas for medicine and society.

Supported in part by Saint John's Cardiovascular Research Center, Torrance, Calif., and the Emergency Medicine Foundation, Dallas.

Source Information

From the UCLA School of Medicine, Los Angeles, and the Department of Emergency Medicine, Harbor–UCLA Medical Center, Torrance, Calif. Address reprint requests to Dr. Niemann at the Department of Emergency Medicine, Harbor–UCLA Medical Center, 1000 West Carson St., Torrance, CA 90509.

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   Wanchun Tang, Max Harry Weil. Cardiac Arrest and Cardiopulmonary Resuscitation. In: Critical Care Medicine. Elsevier, 2008:3-15.
   

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   Tom P. Aufderheide, Keith G. Lurie. (2006) Vital organ blood flow with the impedance threshold device. Critical Care Medicine 34:Suppl, S466-S473
   

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   Daniel M Fatovich, Geoffrey J Dobb, Richard A Clugston. (2004) A pilot randomised trial of thrombolysis in cardiac arrest (The TICA trial). Resuscitation 61:3, 309-313
   

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   S. Holm, E.O. Jørgensen. (2001) Ethical issues in cardiopulmonary resuscitation. Resuscitation 50:2, 135-139
   

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