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Cardiopulmonary resuscitation: Current status
Cardiopulmonary Resuscitation: Current Status Charles W. Otto ESUSCITATION from cardiac arrest in the hospital depends on the rapid response of a well-trained cardiopulmonary resuscitation (CPR) team that usually includes physicians, nurses, respiratory care providers, and pharmacists. The anesthesiologist/critical care physician is usually a team member and, frequently, is expected to be the leader. The team must communicate readily and act in coordination. Published CPR guidelines and courses in basic life support and advanced cardiac life support provide the basic knowledge and framework for effective teamwork. The anesthesiologist/critical care physician must be thoroughly familiar with advanced cardiac life support protocols to function within the team. Team leadership also requires in-depth, current knowledge of physiology, pharmacology, and alternative CPR techniques. The purpose of this review is not to reiterate standard advanced cardiac life support protocols, but to provide the scientific background on which current CPR practice is based. It focuses exclusively on the treatment of cardiac arrest. Unless specifically indicated, other circumstances requiring cardiovascular support, such as shock and dysrhythmias, are not covered. Approximately 40% of patients suffering inhospital cardiac arrest are resuscitated; one quarter of these survive to discharge. Excluding the operating room, the best initial resuscitation rates are found in the intensive care unit (ICU), while the best survival rates are for patients arresting in the emergency department. The in-hospital success is similar to resuscitation and survival rates from out-ofhospital arrest in cities with rapid response emergency medical systems. In out-of-hospital arrests, poor outcomes are associated with (1) long arrest times before CPR is begun, (2) prolonged ventricular fibrillation without definitive therapy, and (3) inadequate coronary and cerebral perfusion during CPR. Optimum survival from ventricular fibrillation is obtained only if basic CPR is started within 4 minutes and defibrillation applied within 8 minutes. A better outcome might be expected for inhospital arrests because of rapid response times and expert personnel. Intercurrent illnesses of hos-
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pitalized patients reduce the likelihood of survival and the arrest victim is more likely to be elderly, a factor that may reduce survival. The cause of arrest associated with the best outcome and the most common cause of out-of-hospital arrest is ventricular fibrillation secondary to myocardial ischemia. This initiating event is less common in hospitalized patients. When applying CPR, attention to the details of effective resuscitation is important. However, it should always be remembered that CPR is only symptomatic therapy and so much attention should not be paid to the mechanics of CPR that search for a treatable cause of the arrest is forgotten. AIRWAY MANAGEMENT The goal of airway management during cardiorespiratory arrest is to provide a clear path for respiratory gas exchange while minimizing gastric insufflation and the risk of pulmonary aspiration. The most commonly used technique for opening the airway is the "head tilt/chin lift" method. If this is ineffective, the "jaw thrust" maneuver is frequently helpful. Oropharyngeal and nasopharyngeal airways are useful for helping maintain an open airway in patients who are not intubated. Care must be used to ensure they are correctly inserted and do not worsen airway obstruction. Insertion in the semiconscious can induce vomiting or laryngospasm. Through the years it has become obvious that effective airway management during CPR is a major problem, even for medical professionals. Many individuals cannot effectively manage a self-inflating resuscitation bag and mask. Larger tidal volumes at lower pressures are delivered by mouthto-mouth or mouth-to-mask ventilation. The bag and mask apparatus is more effective if two indi-
From the Department of Anesthesiology, The University of Arizona College of Medicine, Tucson, AZ Address reprint requests to Department of Anesthesiology, Arizona Health Sciences Center, 1501 N Campbell Ave, PO Box 245114, Tucson, AZ 85724-5114. Copyright 9 1999 by W.B. Saunders Company 0277-0326/99/1801-0004510.00/0
Seminars in Anesthesia, PerioperativeMedicine and Pain, Vol 18, No 1 (March), 1999: pp 71-80
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viduals manage the airway: one to hold the mask and maintain the airway and one to squeeze the bag. Other airway adjuncts, such as the laryngeal mask, the combitube, and the esophageal obturator airway, have been advocated, but, of course, endotracheal intubation provides the best possible airway management. It should be performed in all resuscitations lasting more than a few minutes if a skilled laryngoscopist is available. However, it should not be performed until adequate ventilation by other means (preferably with supplemental oxygen) and circulation by chest compressions have been established.
VENTILATION If the airway remains patent, chest compressions cause substantial air exchange. Early studies in anesthetized humans suggested that the airway would not remain open in the unconscious, leading to the assumption that airway control and artificial ventilation must accompany chest compressions. However, recent human observations and animal studies have challenged this teaching. Data from the Belgian CPCR Registry demonstrate that survival and neurologic outcome is the same if bystanders initiate full basic life support or only do chest compressions. Results with either technique are significantly better than if the bystanders attempt no CPR or only do mouth-to-mouth ventilation. These observations led to the study of the necessity for ventilation during basic life support in animal models. Three recent reports used a swine model with up to 5 minutes of untreated fibrillatory cardiac arrest and 10 minutes of chest compressions without airway control or ventilation. 1-3 All the animals survived for 24 hours and were neurologically normal. A recently completed similar study using an asphyxial cardiac arrest model showed that assisted ventilation during bystander CPR was critical for survival. 4 These observations suggest that when arrest is witnessed, likely to be of cardiac (rather than respiratory) cause, and intubation will be available within a short time, closed chest compressions alone may be as efficacious as compressions and mouth-tomouth ventilation. If these preliminary studies are confirmed, basic life support teaching could be considerably simplified. This could result in improved rates of bystander CPR since studies show that many people are reluctant to provide mouthto-mouth ventilation. Currently, airway manage-
ment and ventilation remain the standard first steps of CPR, especially for those expert in such management. Insufflation of air into the stomach during resuscitation leads to gastric distension, impeding ventilation, and increasing the danger of regurgitation and gastric rupture. In the absence of an endotracheal tube, the relative distribution of gas between the lungs and stomach during mouth-to-mouth or bag-valve-mask ventilation will be determined by the impedance to flow into each compartment, the lung-thorax compliance and the esophageal opening pressure, respectively. Although there are no specific data during human CPR, it is likely that esophageal opening pressure is no higher than it is under anesthesia (approximately 20 cm H20) and that lung thorax-compliance is reduced. If gastric insufflation is to be avoided, inspiratory airway pressures must be kept low. A major cause of increased airway pressures and gastric insufflation is partial airway obstruction by the tongue and pharyngeal tissues. Meticulous attention to maintaining an open airway is necessary during rescue breathing. To cause an obvious increase in the chest of most adults, a tidal volume of 0.8 to 1.2 L will be needed. Even with an open airway, a relatively long inspiratory time is necessary to administer this volume at low pressure. Thus, rescue breaths should be given over 1.5 to 2.0 seconds during a pause in chest compressions. A useful aid in minimizing gastric insufflation is the use of cricoid pressure (Sellick maneuver). Pressure applied over the anterior arch of the cricoid cartilage can prevent air from entering the stomach at airway pressures up to 100 cm H20. Using the head tilt/chin lift method of maintaining an open airway, mouth-to-mouth ventilation is administered by using the hand on the forehead to pinch the nose. The rescuer takes a breath, seals the victim's mouth with his or her mouth, and exhales, watching for the chest to rise. When both hands are being used with the jaw thrust, the cheek can be used to seal the nose. For mouth-to-nose ventilation, the rescuer's lips surround the nose and the lips are held closed. For exhalation, the rescuer removes his or her mouth from the victim, listening for escaping air and taking a breath. When initiating resuscitation, two breaths should be given and breathing should be continued at a rate of 10 to 12 breaths/min. During CPR with one rescuer, a pause for two breaths should be made after each 15 chest
CARDIOPULMONARY RESUSCITATION: CURRENTSTATUS compressions. When there are two rescuers, a 1.5to 2.0-second pause after every fifth chest compression will allow a breath to be given. Exhalation can occur during the next compressions. The best way to ensure adequate ventilation without gastric distension is endotracheal intubation. It is indicated during any prolonged resuscitation. However, other aspects of the resuscitation that might lead to a restoration of spontaneous circulation should not be delayed for intubation. Once an endotracheal tube is in place, ventilation should proceed at approximately 12 breaths/min without concern for gastric distension or synchronizing ventilation with chest compressions.
PHYSIOLOGY OF CIRCULATION DURING CLOSED CHEST COMPRESSION Two theories have been proposed to explain the mechanism by which closed chest compressions cause blood to flow through the circulatory system. They are not mutually exclusive and which predominates in humans continues to be investigated.
Cardiac Pump Mechanism With the original description of closed chest cardiac massage in 1960, Kouwenhoven et al 5 suggested that the heart was compressed between the sternum and spine, resulting in increased intraventricular pressure, closing of the atrioventricular valves, and ejection of blood into the lungs and aorta. During the relaxation phase, negative intrathoracic pressure caused by expansion of the thoracic cage facilitates blood return and aortic pressure results in aortic valve closure and coronary perfusion. This has come to be known as the cardiac pump theory of blood flow during CPR. Support for this theory comes from echocardiography studies that show reduction in ventricular size and mitral valve closure with chest compression during the early stages of CPR. In addition, CPR techniques that incorporate direct sternal compressions, compared with techniques that increase intrathoracic pressure without sternal compressions, result in better tissue blood flow and survival in animals.
Thoracic Pump Mechanism In 1976, Criley et al6 reported a patient undergoing cardiac catheterization who simultaneously developed ventricular fibrillation and an episode of cough/hiccups. With every cough/hiccup, a signif-
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icant arterial pressure was noted and the patient never lost consciousness, even though CPR was not performed. This description of "cough CPR" led to further investigations and the concept of a thoracic pump causing blood flow during CPR. According to this theory, all intrathoracic structures are compressed equally by the increase in intrathoracic pressure resulting from sternal compression. Backward flow through the venous system is prevented by valves in the subclavian and internal jugular veins and by dynamic compression of the veins at the thoracic outlet. Thicker, lesscompressible vessel walls prevent collapse on the arterial side. The heart acts as a passive conduit with the atrioventricular valves remaining open during chest compression. A number of studies and observations support the thoracic pump theory. Angiography during a cough has shown blood flowing through the left heart into the aorta without cardiac compression. Maneuvers that increase intrathoracic pressure (such as simultaneous ventilation and chest compression or abdominal binding) increase arterial pressure and carotid blood flow compared with standard CPR. Artificial circulation adequate to maintain viability can be accomplished with simultaneous ventilation and inflation of vests surrounding the chest and abdomen in experimental animals. It seems clear that fluctuations in intrathoracic pressure play a significant role in blood flow during CPR. It is also likely that the cardiac pump mechanism contributes under some circumstances. Which mechanism predominates probably varies from victim to victim and may vary even during the resuscitation of the same victim.
Distribution of Blood Flow During Cardiopulmonary Resuscitation Whatever the actual mechanism of blood flow, cardiac output is severely reduced during closed chest compressions, ranging from 10% to 33% of prearrest values in experimental animals. Total blood flow also tends to decrease with time during CPR, although changes in technique and the use of epinephrine may help sustain cardiac output. Nearly all the cardiac output is directed to organs above the diaphragm. Brain blood flow is 50% to 90% of normal and myocardial blood flow 20% to 50% of normal while lower extremity and abdominal visceral flow is reduced to less than 5% of
74 normal. All flows tend to decrease with time, but the relative distribution of flow does not change. Epinephrine improves flow to the brain and heart while flow to organs below the diaphragm is unchanged or further reduced.
Gas Transport During Cardiopulmonary Resuscitation During CPR, measurement of blood gases reveals an arterial respiratory alkalosis and a venous respiratory acidosis because the arterial Pco 2 is reduced and the venous Pco 2 is elevated. However, the cause is not pulmonary in origin. The cause of these changes is the reduced cardiac output. During the low flow state of CPR, excretion of carbon dioxide (mL of CO2/min in exhaled gas) is decreased from prearrest levels approximately to the same extent as cardiac output is reduced. This reduced CO 2 excretion is due primarily to shunting of blood flow away from the lower half of the body. The exhaled CO 2 reflects only the metabolism of the part of the body that is being perfused. In the nonperfused areas, CO 2 accumulates during CPR. When normal circulation is restored, the accumulated CO 2 is washed out and a temporary increase in CO 2 excretion is seen. Although CO 2 excretion is reduced during CPR, the mixed venous partial pressure of CO2(Pvco2) usually is increased. Two factors account for this elevation. Buffering acid causes a reduction in serum bicarbonate, so that the same blood CO2 content results in a higher Pvco 2. In addition, the mixed venous CO2 content is elevated. When flow to a tissue is reduced, all the CO2 produced fails to be removed and CO 2 accumulates, increasing the tissue partial pressure of CO 2. This allows more CO 2 to be carried in each aliquot of blood and mixed venous CO z content increases. If flow remains constant, a new equilibrium is established in which all CO 2 produced in the tissue is removed, but at a higher venous CO 2 content and partial pressure. Even though venous blood may have an increased CO 2, the marked reduction in cardiac output with maintained ventilation results in very efficient CO 2 removal. Therefore, arterial CO 2 content and partial pressure (Paco2) usually are reduced during CPR. Decreased pulmonary blood flow during CPR causes lack of perfusion to many nondependent alveoli. The alveolar gas of these lung units have no CO 2. Consequently, mixed alveolar CO 2 (ie,
CHARLES W. 0130 end-tidal CO2) will be very low and correlate poorly with arterial C O 2. However, end-tidal C O 2 does correlate well with cardiac output during CPR. As flow increases, more alveoli become perfused, there is less alveolar dead space, and endtidal CO z measurements increase.
TECHNIQUE OF CLOSED CHEST COMPRESSION Standard chest compression technique consists of the rhythmic application of pressure over the lower half of the sternum. For compressions to be effective in providing blood flow to the brain and heart, the patient must be on a firm surface with the head level with the heart. The rescuer should stand or kneel at the side of the patient so that the hips are on a level with the victim's chest. The heel of one hand is placed on the lower sternum and the other hand is placed on top of the first. Care must be taken that the xiphoid is not pressed into the abdomen, which can lacerate the liver. Pressure on the ribs or costal cartilages rather than the sternum increases the risk of rib fracture. The elbows should be locked in position with the arms straight and the shoulders over the hands. Using the weight of the entire upper body, the compression is delivered straight down with enough force to depress the sternum 3.5 to 5.0 cm. Following maximal compression, pressure is released completely from the chest, but the hands stay in contact with the chest wall maintaining proper hand position for the next thrust. Chest compressions should be performed at a rate of 80 to 100/min. They are most effective if the compression and relaxation phases of the cycle are equal in length. This 50% compression time is easier to achieve at faster compression rates. If a single rescuer is providing CPR, it is recommended that 15 compressions be followed by a pause for two ventilations (1.5 to 2.0 seconds each) followed by 15 more compressions. If there are two rescuers, the person performing chest compressions should pause 1.5 to 2.0 seconds after every five compressions to allow the second rescuer to give a breath. Blood flow during CPR slows rapidly when chest compressions are stopped and recovers slowly when they are restarted. Consequently, following intubation, no pause should be made for ventilation and ventilation should be approximately 12 breaths/min without regard for the compression cycle.
CARDIOPULMONARY RESUSCITATION: CURRENTSTATUS ALTERNATIVE METHODS OF CIRCULATORY SUPPORT Better understanding of circulatory physiology during CPR, especially involving the thoracic pump mechanism, has generated several proposals for alternative techniques in recent years. Most are designed to provide better hemodynamics during CPR and, thus, extend the duration during which CPR can successfully support viability. Unfortunately, none has proven reliably superior to standard techniques and no improvement in survival from cardiac arrest has been consistently demonstrated.
Closed Chest Techniques According to the thoracic pump theory, maneuvers that increase intrathoracic pressure during chest compression should improve blood flow and pressure. Several methods for increasing intrathoracic pressure during CPR have been studied, including simultaneous ventilation and compression, abdominal binding with compression, and the pneumatic antishock garment. Early results indicated improved aortic pressures and carotid blood flows with these techniques. However, subsequent studies failed to demonstrate consistently improved resuscitation success or survival in animals or humans. The increase in aortic pressure seen with these techniques was expected to improve myocardial and cerebral perfusion. However, the elevation in right atrial, intraventricular, and intracranial pressure is equal to or greater than the increase in aortic pressure. The net result is no improvement or diminution of myocardial and cerebral perfusion pressures and blood flows. Three alternative techniques continue to be actively investigated in experimental animals and, to a limited extent, in humans. The pneumatic CPR vest relies entirely on the thoracic pump mechanism of blood flow. Animal studies have shown excellent hemodynamics and the ability to maintain viability for prolonged periods. Improved outcome from cardiac arrest has not been demonstrated in animals. One small clinical study found better aortic and coronary perfusion pressure with the vest compared with standard CPR but survival was not improved. The technique of interposed abdominal compression-CPR uses an additional rescuer to apply manual abdominal compressions during the relaxation phase of chest compressions. Abdominal
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pressure is released when chest compression begins. Initial hemodynamic studies were encouraging, but.a large randomized study of out-of-hospital arrest found no improvement in survival compared with standard CPR. Interest in this technique was rekindled with a report of improved survival from in-hospital cardiac arrest. Further studies of the efficacy and safety of interposed abdominal compression-CPR will be needed to determine whether it has a place in modern CPR practice. The newest proposed alternative technique is called active compression-decompression CPR. With this method, CPR is performed with a suction device applied to the chest over the sternum allowing active decompression. One in-hospital preliminary study found improved immediate resuscitation with the device, but no difference in survival. Two out-of-hospital trials found no difference in immediate resuscitation or survival.
Invasive Techniques Much of the effort spent improving current CPR techniques and investigating new techniques was prompted by the hope that better blood flows would extend the time during which CPR can support viability. Unfortunately, the results have been disappointing. In spite of the occasional success of prolonged resuscitation efforts, it appears that closed chest compressions can sustain most patients only for 15 to 30 minutes. If successful restoration of spontaneous circulation has not occurred in that time, the outcomes are dismal. In contrast to the closed chest techniques, two invasive maneuvers have been shown to be able to maintain cardiac and cerebral viability during long periods of cardiac arrest. In animal models, openchest cardiac massage and cardiopulmonary bypass (through the femoral artery and vein using a membrane oxygenator) can provide better hemodynamics and myocardial and cerebral perfusion than closed chest techniques. Prompt restoration of blood flow and perfusion pressure with cardiopulmonary bypass can provide resuscitation with minimal neurologic deficit after 20 minutes of fibrillatory cardiac arrest in canines. However, to be effective, these techniques must be instituted relatively early (probably within 20 to 30 minutes). If open chest massage is begun after 30 minutes of ineffective closed chest compressions, there is no better survival even though hemodynamics are improved. The need to apply these maneuvers early in
76 an arrest obviously limits the application. In-hospital arrests are circumstances in which the necessary expertise may be available to apply these techniques. However, there is an appropriate reluctance to apply such invasive maneuvers until it is clear that closed-chest techniques are ineffective. Unfortunately, at that point it may be too late for invasive methods to be successful as well. Before invasive procedures can play a greater role in modem CPR, a method must be developed to predict, early in the resuscitation, which patients will or will not respond to closed chest compressions.
ASSESSING THE ADEQUACY OF CIRCULATION DURING CARDIOPULMONARY RESUSCITATION There is an obvious need to assess whether ongoing CPR is generating adequate myocardial and cerebral blood flow for viable resuscitation. The traditional method is to palpate the carotid or femoral pulse during chest compressions. However, a palpable pulse primarily reflects systolic blood pressure. Mean blood pressure correlates better with cardiac output and diastolic pressure is the major determinant of coronary perfusion. Nevertheless, palpation of the pulse remains the only assessment tool available during basic life support. Successful resuscitation in experimental models is associated with myocardial blood flows of 15 to 30 mL/min/100 g. To obtain such flows, closed chest compressions must generate adequate cardiac output and coronary perfusion pressure. During CPR, coronary perfusion occurs primarily during the relaxation phase (diastole) of chest compression. The critical myocardial blood flow is associated with aortic "diastolic" pressure exceeding 40 m m Hg and coronary perfusion pressure (aortic diastolic minus right atrial diastolic pressure) exceeding 25 m m Hg in animal models and humans. When invasive pressure monitoring is available during CPR, it should be used to guide resuscitation efforts. It is untrue that arterial pressure monitoring is unreliable during CPR. If adequate chest compressions are being provided, a functional waveform will be seen in a radial arterial line. If monitored arterial pressures are below the critical levels, adjustments should be made to improve chest compressions and/or additional epinephrine should be administered. Unfortunately, obtaining pressures above the critical levels does not always ensure success. Damage to the myocardiuln from
CHARLES W. OTTO underlying disease may preclude survival no matter how effective the CPR efforts. However, vascular pressures below these levels are associated with poor results, even in patients who may be salvageable. Although invasive pressure monitoring may be the ideal, exhaled end-tidal CO2 is an excellent noninvasive guide to the effectiveness of standard CPR. After intubation, carbon dioxide excretion during CPR is dependent primarily on blood flow rather than ventilation. Since alveolar dead space is large during low flow conditions, end-tidal CO 2 is very low (frequently <10 mm Hg). If cardiac output increases, more alveoli are perfused and end-tidal CO a increases (usually to > 2 0 mm Hg during successful CPR). When spontaneous circulation resumes, the earliest sign is a sudden increase in end-tidal CO z to greater than 40 mm Hg. Within a wide range of cardiac outputs, end-tidal CO 2 during CPR correlates with coronary perfusion pressure, cardiac output, initial resuscitation, and survival. Two studies have shown that endtidal CO 2 measured during human CPR can be used to predict outcome. 7's No patient with an end-tidal CO 2 less than 10 m m Hg could be successfully resuscitated. Thus, in the absence of invasive pressure monitoring, end-tidal CO e monitoring can be used to judge the effectiveness of chest compressions. Attempts should be made to maximize the value by alterations in technique or drug therapy. Sodium bicarbonate administration results in the liberation of CO 2 in the venous blood and a temporary increase in end-tidal CO 2. Therefore, end-tidal CO 2 monitoring will not be useful for judging the effectiveness of chest compressions for 3 to 5 minutes following bicarbonate administration.
DEFIBRILLATION Duration and Electrical Pattern of Fibrillation Ventricular fibrillation is the most common ECG rhythm found in adults experiencing cardiac arrest. The longer fibrillation continues, the more difficult it is to defibrillate and successful resuscitation is is less likely. The fibrillating heart has a high oxygen consumption, which increases myocardial ischemia and decreases the time to irreversible cell damage. The only effective treatment for this dysrhythmia is electrical defibrillation, and the sooner it is applied the higher the rate of successful resuscitation. Thus, conversion of ventricular fi-
CARDIOPULMONARY RESUSCITATION:CURRENTSTATUS brillation to a rhythm capable of restoring spontaneous circulation should be the first priority of any resuscitation attempt. The amplitude (coarseness) of the fibrillatory waves on the electrocardiogram may reflect the severity and duration of the myocardial insult and, thus, have prognostic significance. Low-voltage fibrillation is associated with poor outcome. Increasing myocardial ischemia results in less vigorous fibrillation, reduced amplitude electrical activity, and more difficult defibrillation. Catecholamines with /3-adrenergic activity, such as epinephrine, increase the amplitude of the electrical activity but have no influence on the ability to defibrillate. Consequently, defibrillation should not be postponed for any other therapy but should be completed as soon as the rhythm is diagnosed and the equipment available. The importance of early defibrillation has been demonstrated in numerous studies.
Defibrillators: Energy, Current, and Impedance The defibrillator is a variable transformer that stores a direct current in a capacitor until discharged through the electrodes. Defibrillation is accomplished by the current passing through a critical mass of myocardium causing simultaneous depolarization of the myofibrils. Optimum success of defibrillation is obtained by keeping impedance as low as possible. Many of the important factors in minimizing transthoracic impedance are under the control of the rescuer. Resistance decreases with electrode size, so large paddles (>8 cm diameter) should be used. The greatest impedance is between the metal electrode and skin. This can be reduced slightly by the use of saline-soaked gauze pads or electrocardiogram electrode cream. However, the lowest resistance is obtained with the specially designed defibrillation gels or pastes. Self-adhesive defibrillation/monitor pads also work well when carefully applied. Firm paddle pressure of at least 11 kg reduces resistance by improving electrode-skin contact and by expelling air from the lung. Transthoracic impedance is reduced by successive shocks. This factor may partially explain why additional shocks of the same energy may succeed when previous shocks did not. If relatively high energy (>300 J) shocks are used with reasonable attention to proper technique, resistance is probably of little clinical significance.
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For lower energy shocks, great care should be taken to minimize resistance.
Energy Requirements and Adverse Effects The incidence and severity of myocardial damage from defibrillation in humans is not clear. Repeated high level shocks in animals result in dysrhythmias, electrocardiographic changes and myocardial necrosis. Whether such injuries occur in humans is unknown, although slight elevations in creatine kinase MB fractions have been reported after cardioversions with high energies. It would seem prudent to keep energy levels as low as possible during defibrillation attempts. A general relationship exists between body size and energy requirements for defibrillation. Children need lower energies than adults, perhaps as low as 0.5 J/kg, although the recommended pediattic dose is 2 J/kg. In adults, body size does not seem to be a clinically important variable. Multiple studies have demonstrated that using relatively low level initial shocks in adults is as successful as beginning with higher energy. Therefore, it is currently recommended that the initial shock be given at 200 J followed by a second shock at 200 to 300 J if the first is unsuccessful. If both fail to defibrillate the patient, additional shocks should be given at 300 to 360 J.
DRUG THERAPY
Catecholamines and Vasopressors The only drugs universally accepted as being useful during CPR are the vasopressors. Epinephrine has been used in resuscitation since the 1890s and has been the vasopressor of choice in modem CPR since the studies of Redding and Pearson in the 1960s. 9 The efficacy of epinephrine lies entirely in its a-adrenergic properties. Peripheral vasoconstriction leads to an increase in aortic diastolic pressure causing an increase in coronary perfusion pressure and myocardial blood flow. It is tempting to invoke the/3-adrenergic properties of cardiac stimulation to explain the success of epinephrine. However, animal studies have demonstrated that all strong t~-adrenergic drugs (epinephrine, phenylephrine, methoxamine, dopamine, norepinephrine) are equally successful in aiding resuscitation regardless of the /3-adrenergic potency. /3-Adrenergic agonists without alpha activity (isoproterenol, dobutamine) are no better than
78 placebo, c~-Adrenergic blockade precludes resuscitation while /3-adrenergic blockade has no effect on the ability to restore spontaneous circulation. It is generally believed that the ability of epinephrine to increase the amplitude of ventricular fibrillation (a/3-adrenergic effect) makes defibrillation easier. In fact, animal studies have shown that epinephrine does not improve the success of or decrease the energy necessary for defibrillation. Retrospective clinical studies have shown no effect of epinephrine on defibrillation success. The/3-adrenergic effects of epinephrine are potentially deleterious during cardiac arrest. In the fibrillating heart, epinephrine increases myocardial oxygen consumption. Myocardial lactate production in the fibrillating heart is unchanged after epinephrine administration during CPR, suggesting that the increased coronary blood flow does not improve the oxygen supply to demand ratio. Large doses of epinephrine given during CPR increase deaths in swine early after resuscitation due to tachyarrhythmias and hypertension. In spite of these theoretical considerations, survival and neurologic outcome studies have shown no difference when epinephrine is compared with a pure a-agonist (methoxamine or phenylephrine) during CPR in animals or humans. Because of the long experience with epinephrine, it remains the vasopressor of choice in CPR. It should be administered whenever resuscitation has not occurred after adequate chest compressions and ventilation have been started and defibrillation attempted, if appropriate.
Epinephrine Dose When added to chest compressions, epinephrine helps develop the critical coronary perfusion pressure necessary to provide enough myocardial blood flow for restoration of spontaneous circulation. The standard dose used in animals and humans for many years has been 0.5 to 1.0 mg intravenously. On a weight basis, this dose is approximately 0.1 mg/kg in animals but only 0.015 mg/kg in humans. In some animal models, the standard dose of epinephrine (0.02 mg/kg) is insufficient to improve coronary perfusion pressure and blood flow, but a high dose (0.2 mg/kg) improves hemodynamics to levels compatible with successful resuscitation. Therefore, it has been suggested that higher doses of epinephrine in human CPR might improve myocardial and cerebral perfusion and improve success of resuscitation.
CHARLESW. 01-10 There are several case reports and a series of children (with historical controls) that demonstrated return of spontaneous circulation when large doses (0.1 to 0.2 mg/kg) of epinephrine were given to patients who had failed resuscitation with standard doses. Outcome studies prospectively comparing standard and high-dose epinephrine have not demonstrated conclusively that higher doses will improve survival. There are two randomized blinded studies of standard and high-dose epinephrine in a swine cardiac arrest model. There was no difference in 24-hour survival or neurologic outcome, but more of the high-dose animals died in the early postresuscitation period due to a hyperdynamic state. There are four published studies comparing standard doses (1 to 2 rag) to high doses (5 to 18 mg) of epinephrine in human CPR. All are prospective randomized double-blind clinical trials in cardiac arrest victims, primarily out-of-hospital. The resuits of two of the studies suggested there may be an improvement in immediate resuscitation with high-dose epinephrine while the other two found no difference. None of the studies found any improvement in survival to hospital discharge. High doses of epinephrine apparently are not needed as initial therapy for most cardiac arrests and potentially could be deleterious under some circumstances. However, the successful case reports were in patients with prolonged CPR and the high doses were given as "rescue" therapy when standard doses had failed. This may be the appropriate place for higher doses of epinephrine in CPR practice. Current recommendations are to give 1 mg intravenously every 3 to 5 minutes in the adult. If this dose seems ineffective, higher doses (3 to 8 rag) should be considered.
Sodium Bicarbonate Considerable concern has been expressed in recent years over the implications of gas transport physiology for acid-base homeostasis during CPR. Intravenous sodium bicarbonate combines with hydrogen ion resulting in the liberation of CO 2. The arterial Pco 2 is temporarily elevated until the excess CO 2 is eliminated through the lungs. It is only with the elimination of the volatile acid (CO2) that bicarbonate becomes an effective buffer. It has been suggested that sodium bicarbonate administration during CPR could be harmful, since tissue acidosis is primarily caused by the low blood flow
CARDIOPULMONARY RESUSCITATION:CURRENTSTATUS and accumulation of C O 2 in the tissues. C O 2 readily diffuses across cell membranes and the blood-brain barrier while bicarbonate diffuses much more slowly. Thus, it is possible that sodium bicarbonate administration could result in a "paradoxical" worsening of intracellular and cerebral acidosis by further raising intracellular and cerebral CO 2 without a balancing increase in bicarbonate. Direct evidence of this occurring during CPR is lacking at this time. Measurement of myocardial intracellular pH during sodium bicarbonate administration did not detect a worsening acidosis. Similarly, recent studies of cerebral spinal fluid pH found no change following administration of clinically relevant sodium bicarbonate doses. Therefore, paradoxical acidosis remains a concern primarily on theoretical grounds. The usefulness of sodium bicarbonate therapy during CPR also rests primarily on theoretical grounds. Acidosis lowers fibrillation threshold and impairs the physiologic response to catecholamines. There have been some recent reports that sodium bicarbonate administration may improve resuscitation from prolonged arrest without CPR in dogs. However, conclusive evidence that sodium bicarbonate improves survival will require additional studies. In contrast, hypernatremia, hyperosmolarity, and metabolic alkalosis are well-documented after CPR when sodium bicarbonate is used. These abnormalities are associated with a low resuscitation rate and poor survival. Therefore, current knowledge suggests that sodium bicarbonate should be used judiciously during CPR, restricting its use primarily to arrests associated with hyperkalemia, severe pre-existing metabolic acidosis, and tricyclic or phenobarbital overdose. It may be considered for use in protracted resuscitation attempts after other modalities have been instituted. If it is used, the risk of paradoxical acidosis can be reduced by giving the bicarbonate slowly rather than by rapid intravenous bolus.
Routes of Administration The preferred route of administration of all drugs during CPR is intravenous and the doses referred to in this report are for intravenous use. The most rapid and highest drug levels occur with administration into a central vein. Therefore, when a central venous catheter is available
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during a cardiac arrest, it should be used for drug therapy. However, peripheral intravenous administration also is effective. The antecubital or external jugular vein should be the site of first choice for starting an infusion during resuscitation because starting a central line usually necessitates stopping CPR. Sites in the upper extremity and neck are preferred because of the paucity of blood flow below the diaphragm during CPR. Drugs administered in the lower extremity may be extremely delayed or not reach the sites of action. Even in the upper extremity, drugs may require 1 to 2 minutes to reach the central circulation. Onset of action may be speeded if a drug bolus is followed by a 20- to 30-mL bolus of intravenous fluid. Epinephrine, lidocaine, and atropine do not injure the lungs and can be absorbed from the tracheal mucosa. Therefore, if intravenous access cannot be established, the endotracheal route provides an alternative for these drugs following intubation. Sodium bicarbonate should not be given by this route. The time to effect and drug levels achieved are very inconsistent using this route during CPR. Studies have demonstrated that volumes of 5 to 10 mL need to be delivered to have reasonable uptake. It is likely that higher doses of the drugs need to be used via this route; 2 to 2.5 times the intravenous dose is recommended currently. Studies conflict on whether deep injection is better than simple instillation in the tube.
REFERENCES 1. Berg RA, Kern KB, Sanders AB, et al: Bystander cardiopulmonary resuscitation. Is ventilation necessary? Circulation 88:1907-1915, 1993 2. Berg RA, Wilcoxson D, Hilwig RW, et al: The need for ventilatory support during bystander cardiopulmonary resuscitation. Ann Emerg Med 26:342-350, 1995 3. Berg RA, Kern KB, Hilwig RW, et al: Assisted ventilation does not improve outcome in a porcine model of single-rescuer bystander CPR. Circulation 95:1635-1641, 1997 4. Berg RA, Hilwig RW, Kern KB, et al: Assisted ventilation during "bystander" CPR improves outcome in a swine model of pediatric asphyxial cardiac arrest. Circulation 1999 (in press) 5. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closedchest cardiac massage. JAMA 173:1064-1067, 1960 6. Criley JM, Blaufuss AH, Kissel GL: Cough-induced cardiac compression. Self-administration form of cardiopulmonary resuscitation. JAMA 236:1246-1250, 1976 7. Sanders AB, Kern KB, Otto CW, et al: End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. A prognostic indicator for survival. JAMA 262:1347-1351, 1989
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8. Levine RL, Wayne MA, Miller CC: End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med 337:301-306, 1997 9. Redding JS, Pearson JW: Evaluation of drugs for cardiac resuscitation. Anesthesiology 24:203-207, 1963
SUGGESTED READING American Heart Association: Textbook of Advanced Cardiac Life Support. Dallas, TX, American Heart Association, 1994, pp 1-285 Emergency Cardiac Care Committee and Subcommittees, American Heart Association: Guidelines for cardiopulmonary
resuscitation and emergency cardiac care. JAMA 268:21712295, 1992 Otto CW: Cardiopuhnonary resuscitation, in Barash PG, Cullen BF, Stoelting RK (eds): Clinical Anesthesia (ed 3). Philadelphia, PA, Lippencott-Raven, 1997, pp 1389-1410 Otto CW: Cardiopulmonary resuscitation, in Longnecker DE, Tinker JH, Morgan GE (eds): Principles and Practice of Anesthesiology. St Louis, MO, Mosby-Yearbook, 1998, pp 647-679 Proceedings of the 1985 National Conference on Standards and Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiac Care. Montgomery WH (ed): Circulation Supplement 74:IV-l-IV-153, 1986 (suppl)
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pitalized patients reduce the likelihood of survival and the arrest victim is more likely to be elderly, a factor that may reduce survival. The cause of arrest associated with the best outcome and the most common cause of out-of-hospital arrest is ventricular fibrillation secondary to myocardial ischemia. This initiating event is less common in hospitalized patients. When applying CPR, attention to the details of effective resuscitation is important. However, it should always be remembered that CPR is only symptomatic therapy and so much attention should not be paid to the mechanics of CPR that search for a treatable cause of the arrest is forgotten. AIRWAY MANAGEMENT The goal of airway management during cardiorespiratory arrest is to provide a clear path for respiratory gas exchange while minimizing gastric insufflation and the risk of pulmonary aspiration. The most commonly used technique for opening the airway is the "head tilt/chin lift" method. If this is ineffective, the "jaw thrust" maneuver is frequently helpful. Oropharyngeal and nasopharyngeal airways are useful for helping maintain an open airway in patients who are not intubated. Care must be used to ensure they are correctly inserted and do not worsen airway obstruction. Insertion in the semiconscious can induce vomiting or laryngospasm. Through the years it has become obvious that effective airway management during CPR is a major problem, even for medical professionals. Many individuals cannot effectively manage a self-inflating resuscitation bag and mask. Larger tidal volumes at lower pressures are delivered by mouthto-mouth or mouth-to-mask ventilation. The bag and mask apparatus is more effective if two indi-
From the Department of Anesthesiology, The University of Arizona College of Medicine, Tucson, AZ Address reprint requests to Department of Anesthesiology, Arizona Health Sciences Center, 1501 N Campbell Ave, PO Box 245114, Tucson, AZ 85724-5114. Copyright 9 1999 by W.B. Saunders Company 0277-0326/99/1801-0004510.00/0
Seminars in Anesthesia, PerioperativeMedicine and Pain, Vol 18, No 1 (March), 1999: pp 71-80
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viduals manage the airway: one to hold the mask and maintain the airway and one to squeeze the bag. Other airway adjuncts, such as the laryngeal mask, the combitube, and the esophageal obturator airway, have been advocated, but, of course, endotracheal intubation provides the best possible airway management. It should be performed in all resuscitations lasting more than a few minutes if a skilled laryngoscopist is available. However, it should not be performed until adequate ventilation by other means (preferably with supplemental oxygen) and circulation by chest compressions have been established.
VENTILATION If the airway remains patent, chest compressions cause substantial air exchange. Early studies in anesthetized humans suggested that the airway would not remain open in the unconscious, leading to the assumption that airway control and artificial ventilation must accompany chest compressions. However, recent human observations and animal studies have challenged this teaching. Data from the Belgian CPCR Registry demonstrate that survival and neurologic outcome is the same if bystanders initiate full basic life support or only do chest compressions. Results with either technique are significantly better than if the bystanders attempt no CPR or only do mouth-to-mouth ventilation. These observations led to the study of the necessity for ventilation during basic life support in animal models. Three recent reports used a swine model with up to 5 minutes of untreated fibrillatory cardiac arrest and 10 minutes of chest compressions without airway control or ventilation. 1-3 All the animals survived for 24 hours and were neurologically normal. A recently completed similar study using an asphyxial cardiac arrest model showed that assisted ventilation during bystander CPR was critical for survival. 4 These observations suggest that when arrest is witnessed, likely to be of cardiac (rather than respiratory) cause, and intubation will be available within a short time, closed chest compressions alone may be as efficacious as compressions and mouth-tomouth ventilation. If these preliminary studies are confirmed, basic life support teaching could be considerably simplified. This could result in improved rates of bystander CPR since studies show that many people are reluctant to provide mouthto-mouth ventilation. Currently, airway manage-
ment and ventilation remain the standard first steps of CPR, especially for those expert in such management. Insufflation of air into the stomach during resuscitation leads to gastric distension, impeding ventilation, and increasing the danger of regurgitation and gastric rupture. In the absence of an endotracheal tube, the relative distribution of gas between the lungs and stomach during mouth-to-mouth or bag-valve-mask ventilation will be determined by the impedance to flow into each compartment, the lung-thorax compliance and the esophageal opening pressure, respectively. Although there are no specific data during human CPR, it is likely that esophageal opening pressure is no higher than it is under anesthesia (approximately 20 cm H20) and that lung thorax-compliance is reduced. If gastric insufflation is to be avoided, inspiratory airway pressures must be kept low. A major cause of increased airway pressures and gastric insufflation is partial airway obstruction by the tongue and pharyngeal tissues. Meticulous attention to maintaining an open airway is necessary during rescue breathing. To cause an obvious increase in the chest of most adults, a tidal volume of 0.8 to 1.2 L will be needed. Even with an open airway, a relatively long inspiratory time is necessary to administer this volume at low pressure. Thus, rescue breaths should be given over 1.5 to 2.0 seconds during a pause in chest compressions. A useful aid in minimizing gastric insufflation is the use of cricoid pressure (Sellick maneuver). Pressure applied over the anterior arch of the cricoid cartilage can prevent air from entering the stomach at airway pressures up to 100 cm H20. Using the head tilt/chin lift method of maintaining an open airway, mouth-to-mouth ventilation is administered by using the hand on the forehead to pinch the nose. The rescuer takes a breath, seals the victim's mouth with his or her mouth, and exhales, watching for the chest to rise. When both hands are being used with the jaw thrust, the cheek can be used to seal the nose. For mouth-to-nose ventilation, the rescuer's lips surround the nose and the lips are held closed. For exhalation, the rescuer removes his or her mouth from the victim, listening for escaping air and taking a breath. When initiating resuscitation, two breaths should be given and breathing should be continued at a rate of 10 to 12 breaths/min. During CPR with one rescuer, a pause for two breaths should be made after each 15 chest
CARDIOPULMONARY RESUSCITATION: CURRENTSTATUS compressions. When there are two rescuers, a 1.5to 2.0-second pause after every fifth chest compression will allow a breath to be given. Exhalation can occur during the next compressions. The best way to ensure adequate ventilation without gastric distension is endotracheal intubation. It is indicated during any prolonged resuscitation. However, other aspects of the resuscitation that might lead to a restoration of spontaneous circulation should not be delayed for intubation. Once an endotracheal tube is in place, ventilation should proceed at approximately 12 breaths/min without concern for gastric distension or synchronizing ventilation with chest compressions.
PHYSIOLOGY OF CIRCULATION DURING CLOSED CHEST COMPRESSION Two theories have been proposed to explain the mechanism by which closed chest compressions cause blood to flow through the circulatory system. They are not mutually exclusive and which predominates in humans continues to be investigated.
Cardiac Pump Mechanism With the original description of closed chest cardiac massage in 1960, Kouwenhoven et al 5 suggested that the heart was compressed between the sternum and spine, resulting in increased intraventricular pressure, closing of the atrioventricular valves, and ejection of blood into the lungs and aorta. During the relaxation phase, negative intrathoracic pressure caused by expansion of the thoracic cage facilitates blood return and aortic pressure results in aortic valve closure and coronary perfusion. This has come to be known as the cardiac pump theory of blood flow during CPR. Support for this theory comes from echocardiography studies that show reduction in ventricular size and mitral valve closure with chest compression during the early stages of CPR. In addition, CPR techniques that incorporate direct sternal compressions, compared with techniques that increase intrathoracic pressure without sternal compressions, result in better tissue blood flow and survival in animals.
Thoracic Pump Mechanism In 1976, Criley et al6 reported a patient undergoing cardiac catheterization who simultaneously developed ventricular fibrillation and an episode of cough/hiccups. With every cough/hiccup, a signif-
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icant arterial pressure was noted and the patient never lost consciousness, even though CPR was not performed. This description of "cough CPR" led to further investigations and the concept of a thoracic pump causing blood flow during CPR. According to this theory, all intrathoracic structures are compressed equally by the increase in intrathoracic pressure resulting from sternal compression. Backward flow through the venous system is prevented by valves in the subclavian and internal jugular veins and by dynamic compression of the veins at the thoracic outlet. Thicker, lesscompressible vessel walls prevent collapse on the arterial side. The heart acts as a passive conduit with the atrioventricular valves remaining open during chest compression. A number of studies and observations support the thoracic pump theory. Angiography during a cough has shown blood flowing through the left heart into the aorta without cardiac compression. Maneuvers that increase intrathoracic pressure (such as simultaneous ventilation and chest compression or abdominal binding) increase arterial pressure and carotid blood flow compared with standard CPR. Artificial circulation adequate to maintain viability can be accomplished with simultaneous ventilation and inflation of vests surrounding the chest and abdomen in experimental animals. It seems clear that fluctuations in intrathoracic pressure play a significant role in blood flow during CPR. It is also likely that the cardiac pump mechanism contributes under some circumstances. Which mechanism predominates probably varies from victim to victim and may vary even during the resuscitation of the same victim.
Distribution of Blood Flow During Cardiopulmonary Resuscitation Whatever the actual mechanism of blood flow, cardiac output is severely reduced during closed chest compressions, ranging from 10% to 33% of prearrest values in experimental animals. Total blood flow also tends to decrease with time during CPR, although changes in technique and the use of epinephrine may help sustain cardiac output. Nearly all the cardiac output is directed to organs above the diaphragm. Brain blood flow is 50% to 90% of normal and myocardial blood flow 20% to 50% of normal while lower extremity and abdominal visceral flow is reduced to less than 5% of
74 normal. All flows tend to decrease with time, but the relative distribution of flow does not change. Epinephrine improves flow to the brain and heart while flow to organs below the diaphragm is unchanged or further reduced.
Gas Transport During Cardiopulmonary Resuscitation During CPR, measurement of blood gases reveals an arterial respiratory alkalosis and a venous respiratory acidosis because the arterial Pco 2 is reduced and the venous Pco 2 is elevated. However, the cause is not pulmonary in origin. The cause of these changes is the reduced cardiac output. During the low flow state of CPR, excretion of carbon dioxide (mL of CO2/min in exhaled gas) is decreased from prearrest levels approximately to the same extent as cardiac output is reduced. This reduced CO 2 excretion is due primarily to shunting of blood flow away from the lower half of the body. The exhaled CO 2 reflects only the metabolism of the part of the body that is being perfused. In the nonperfused areas, CO 2 accumulates during CPR. When normal circulation is restored, the accumulated CO 2 is washed out and a temporary increase in CO 2 excretion is seen. Although CO 2 excretion is reduced during CPR, the mixed venous partial pressure of CO2(Pvco2) usually is increased. Two factors account for this elevation. Buffering acid causes a reduction in serum bicarbonate, so that the same blood CO2 content results in a higher Pvco 2. In addition, the mixed venous CO2 content is elevated. When flow to a tissue is reduced, all the CO2 produced fails to be removed and CO 2 accumulates, increasing the tissue partial pressure of CO 2. This allows more CO 2 to be carried in each aliquot of blood and mixed venous CO z content increases. If flow remains constant, a new equilibrium is established in which all CO 2 produced in the tissue is removed, but at a higher venous CO 2 content and partial pressure. Even though venous blood may have an increased CO 2, the marked reduction in cardiac output with maintained ventilation results in very efficient CO 2 removal. Therefore, arterial CO 2 content and partial pressure (Paco2) usually are reduced during CPR. Decreased pulmonary blood flow during CPR causes lack of perfusion to many nondependent alveoli. The alveolar gas of these lung units have no CO 2. Consequently, mixed alveolar CO 2 (ie,
CHARLES W. 0130 end-tidal CO2) will be very low and correlate poorly with arterial C O 2. However, end-tidal C O 2 does correlate well with cardiac output during CPR. As flow increases, more alveoli become perfused, there is less alveolar dead space, and endtidal CO z measurements increase.
TECHNIQUE OF CLOSED CHEST COMPRESSION Standard chest compression technique consists of the rhythmic application of pressure over the lower half of the sternum. For compressions to be effective in providing blood flow to the brain and heart, the patient must be on a firm surface with the head level with the heart. The rescuer should stand or kneel at the side of the patient so that the hips are on a level with the victim's chest. The heel of one hand is placed on the lower sternum and the other hand is placed on top of the first. Care must be taken that the xiphoid is not pressed into the abdomen, which can lacerate the liver. Pressure on the ribs or costal cartilages rather than the sternum increases the risk of rib fracture. The elbows should be locked in position with the arms straight and the shoulders over the hands. Using the weight of the entire upper body, the compression is delivered straight down with enough force to depress the sternum 3.5 to 5.0 cm. Following maximal compression, pressure is released completely from the chest, but the hands stay in contact with the chest wall maintaining proper hand position for the next thrust. Chest compressions should be performed at a rate of 80 to 100/min. They are most effective if the compression and relaxation phases of the cycle are equal in length. This 50% compression time is easier to achieve at faster compression rates. If a single rescuer is providing CPR, it is recommended that 15 compressions be followed by a pause for two ventilations (1.5 to 2.0 seconds each) followed by 15 more compressions. If there are two rescuers, the person performing chest compressions should pause 1.5 to 2.0 seconds after every five compressions to allow the second rescuer to give a breath. Blood flow during CPR slows rapidly when chest compressions are stopped and recovers slowly when they are restarted. Consequently, following intubation, no pause should be made for ventilation and ventilation should be approximately 12 breaths/min without regard for the compression cycle.
CARDIOPULMONARY RESUSCITATION: CURRENTSTATUS ALTERNATIVE METHODS OF CIRCULATORY SUPPORT Better understanding of circulatory physiology during CPR, especially involving the thoracic pump mechanism, has generated several proposals for alternative techniques in recent years. Most are designed to provide better hemodynamics during CPR and, thus, extend the duration during which CPR can successfully support viability. Unfortunately, none has proven reliably superior to standard techniques and no improvement in survival from cardiac arrest has been consistently demonstrated.
Closed Chest Techniques According to the thoracic pump theory, maneuvers that increase intrathoracic pressure during chest compression should improve blood flow and pressure. Several methods for increasing intrathoracic pressure during CPR have been studied, including simultaneous ventilation and compression, abdominal binding with compression, and the pneumatic antishock garment. Early results indicated improved aortic pressures and carotid blood flows with these techniques. However, subsequent studies failed to demonstrate consistently improved resuscitation success or survival in animals or humans. The increase in aortic pressure seen with these techniques was expected to improve myocardial and cerebral perfusion. However, the elevation in right atrial, intraventricular, and intracranial pressure is equal to or greater than the increase in aortic pressure. The net result is no improvement or diminution of myocardial and cerebral perfusion pressures and blood flows. Three alternative techniques continue to be actively investigated in experimental animals and, to a limited extent, in humans. The pneumatic CPR vest relies entirely on the thoracic pump mechanism of blood flow. Animal studies have shown excellent hemodynamics and the ability to maintain viability for prolonged periods. Improved outcome from cardiac arrest has not been demonstrated in animals. One small clinical study found better aortic and coronary perfusion pressure with the vest compared with standard CPR but survival was not improved. The technique of interposed abdominal compression-CPR uses an additional rescuer to apply manual abdominal compressions during the relaxation phase of chest compressions. Abdominal
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pressure is released when chest compression begins. Initial hemodynamic studies were encouraging, but.a large randomized study of out-of-hospital arrest found no improvement in survival compared with standard CPR. Interest in this technique was rekindled with a report of improved survival from in-hospital cardiac arrest. Further studies of the efficacy and safety of interposed abdominal compression-CPR will be needed to determine whether it has a place in modern CPR practice. The newest proposed alternative technique is called active compression-decompression CPR. With this method, CPR is performed with a suction device applied to the chest over the sternum allowing active decompression. One in-hospital preliminary study found improved immediate resuscitation with the device, but no difference in survival. Two out-of-hospital trials found no difference in immediate resuscitation or survival.
Invasive Techniques Much of the effort spent improving current CPR techniques and investigating new techniques was prompted by the hope that better blood flows would extend the time during which CPR can support viability. Unfortunately, the results have been disappointing. In spite of the occasional success of prolonged resuscitation efforts, it appears that closed chest compressions can sustain most patients only for 15 to 30 minutes. If successful restoration of spontaneous circulation has not occurred in that time, the outcomes are dismal. In contrast to the closed chest techniques, two invasive maneuvers have been shown to be able to maintain cardiac and cerebral viability during long periods of cardiac arrest. In animal models, openchest cardiac massage and cardiopulmonary bypass (through the femoral artery and vein using a membrane oxygenator) can provide better hemodynamics and myocardial and cerebral perfusion than closed chest techniques. Prompt restoration of blood flow and perfusion pressure with cardiopulmonary bypass can provide resuscitation with minimal neurologic deficit after 20 minutes of fibrillatory cardiac arrest in canines. However, to be effective, these techniques must be instituted relatively early (probably within 20 to 30 minutes). If open chest massage is begun after 30 minutes of ineffective closed chest compressions, there is no better survival even though hemodynamics are improved. The need to apply these maneuvers early in
76 an arrest obviously limits the application. In-hospital arrests are circumstances in which the necessary expertise may be available to apply these techniques. However, there is an appropriate reluctance to apply such invasive maneuvers until it is clear that closed-chest techniques are ineffective. Unfortunately, at that point it may be too late for invasive methods to be successful as well. Before invasive procedures can play a greater role in modem CPR, a method must be developed to predict, early in the resuscitation, which patients will or will not respond to closed chest compressions.
ASSESSING THE ADEQUACY OF CIRCULATION DURING CARDIOPULMONARY RESUSCITATION There is an obvious need to assess whether ongoing CPR is generating adequate myocardial and cerebral blood flow for viable resuscitation. The traditional method is to palpate the carotid or femoral pulse during chest compressions. However, a palpable pulse primarily reflects systolic blood pressure. Mean blood pressure correlates better with cardiac output and diastolic pressure is the major determinant of coronary perfusion. Nevertheless, palpation of the pulse remains the only assessment tool available during basic life support. Successful resuscitation in experimental models is associated with myocardial blood flows of 15 to 30 mL/min/100 g. To obtain such flows, closed chest compressions must generate adequate cardiac output and coronary perfusion pressure. During CPR, coronary perfusion occurs primarily during the relaxation phase (diastole) of chest compression. The critical myocardial blood flow is associated with aortic "diastolic" pressure exceeding 40 m m Hg and coronary perfusion pressure (aortic diastolic minus right atrial diastolic pressure) exceeding 25 m m Hg in animal models and humans. When invasive pressure monitoring is available during CPR, it should be used to guide resuscitation efforts. It is untrue that arterial pressure monitoring is unreliable during CPR. If adequate chest compressions are being provided, a functional waveform will be seen in a radial arterial line. If monitored arterial pressures are below the critical levels, adjustments should be made to improve chest compressions and/or additional epinephrine should be administered. Unfortunately, obtaining pressures above the critical levels does not always ensure success. Damage to the myocardiuln from
CHARLES W. OTTO underlying disease may preclude survival no matter how effective the CPR efforts. However, vascular pressures below these levels are associated with poor results, even in patients who may be salvageable. Although invasive pressure monitoring may be the ideal, exhaled end-tidal CO2 is an excellent noninvasive guide to the effectiveness of standard CPR. After intubation, carbon dioxide excretion during CPR is dependent primarily on blood flow rather than ventilation. Since alveolar dead space is large during low flow conditions, end-tidal CO 2 is very low (frequently <10 mm Hg). If cardiac output increases, more alveoli are perfused and end-tidal CO a increases (usually to > 2 0 mm Hg during successful CPR). When spontaneous circulation resumes, the earliest sign is a sudden increase in end-tidal CO z to greater than 40 mm Hg. Within a wide range of cardiac outputs, end-tidal CO 2 during CPR correlates with coronary perfusion pressure, cardiac output, initial resuscitation, and survival. Two studies have shown that endtidal CO 2 measured during human CPR can be used to predict outcome. 7's No patient with an end-tidal CO 2 less than 10 m m Hg could be successfully resuscitated. Thus, in the absence of invasive pressure monitoring, end-tidal CO e monitoring can be used to judge the effectiveness of chest compressions. Attempts should be made to maximize the value by alterations in technique or drug therapy. Sodium bicarbonate administration results in the liberation of CO 2 in the venous blood and a temporary increase in end-tidal CO 2. Therefore, end-tidal CO 2 monitoring will not be useful for judging the effectiveness of chest compressions for 3 to 5 minutes following bicarbonate administration.
DEFIBRILLATION Duration and Electrical Pattern of Fibrillation Ventricular fibrillation is the most common ECG rhythm found in adults experiencing cardiac arrest. The longer fibrillation continues, the more difficult it is to defibrillate and successful resuscitation is is less likely. The fibrillating heart has a high oxygen consumption, which increases myocardial ischemia and decreases the time to irreversible cell damage. The only effective treatment for this dysrhythmia is electrical defibrillation, and the sooner it is applied the higher the rate of successful resuscitation. Thus, conversion of ventricular fi-
CARDIOPULMONARY RESUSCITATION:CURRENTSTATUS brillation to a rhythm capable of restoring spontaneous circulation should be the first priority of any resuscitation attempt. The amplitude (coarseness) of the fibrillatory waves on the electrocardiogram may reflect the severity and duration of the myocardial insult and, thus, have prognostic significance. Low-voltage fibrillation is associated with poor outcome. Increasing myocardial ischemia results in less vigorous fibrillation, reduced amplitude electrical activity, and more difficult defibrillation. Catecholamines with /3-adrenergic activity, such as epinephrine, increase the amplitude of the electrical activity but have no influence on the ability to defibrillate. Consequently, defibrillation should not be postponed for any other therapy but should be completed as soon as the rhythm is diagnosed and the equipment available. The importance of early defibrillation has been demonstrated in numerous studies.
Defibrillators: Energy, Current, and Impedance The defibrillator is a variable transformer that stores a direct current in a capacitor until discharged through the electrodes. Defibrillation is accomplished by the current passing through a critical mass of myocardium causing simultaneous depolarization of the myofibrils. Optimum success of defibrillation is obtained by keeping impedance as low as possible. Many of the important factors in minimizing transthoracic impedance are under the control of the rescuer. Resistance decreases with electrode size, so large paddles (>8 cm diameter) should be used. The greatest impedance is between the metal electrode and skin. This can be reduced slightly by the use of saline-soaked gauze pads or electrocardiogram electrode cream. However, the lowest resistance is obtained with the specially designed defibrillation gels or pastes. Self-adhesive defibrillation/monitor pads also work well when carefully applied. Firm paddle pressure of at least 11 kg reduces resistance by improving electrode-skin contact and by expelling air from the lung. Transthoracic impedance is reduced by successive shocks. This factor may partially explain why additional shocks of the same energy may succeed when previous shocks did not. If relatively high energy (>300 J) shocks are used with reasonable attention to proper technique, resistance is probably of little clinical significance.
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For lower energy shocks, great care should be taken to minimize resistance.
Energy Requirements and Adverse Effects The incidence and severity of myocardial damage from defibrillation in humans is not clear. Repeated high level shocks in animals result in dysrhythmias, electrocardiographic changes and myocardial necrosis. Whether such injuries occur in humans is unknown, although slight elevations in creatine kinase MB fractions have been reported after cardioversions with high energies. It would seem prudent to keep energy levels as low as possible during defibrillation attempts. A general relationship exists between body size and energy requirements for defibrillation. Children need lower energies than adults, perhaps as low as 0.5 J/kg, although the recommended pediattic dose is 2 J/kg. In adults, body size does not seem to be a clinically important variable. Multiple studies have demonstrated that using relatively low level initial shocks in adults is as successful as beginning with higher energy. Therefore, it is currently recommended that the initial shock be given at 200 J followed by a second shock at 200 to 300 J if the first is unsuccessful. If both fail to defibrillate the patient, additional shocks should be given at 300 to 360 J.
DRUG THERAPY
Catecholamines and Vasopressors The only drugs universally accepted as being useful during CPR are the vasopressors. Epinephrine has been used in resuscitation since the 1890s and has been the vasopressor of choice in modem CPR since the studies of Redding and Pearson in the 1960s. 9 The efficacy of epinephrine lies entirely in its a-adrenergic properties. Peripheral vasoconstriction leads to an increase in aortic diastolic pressure causing an increase in coronary perfusion pressure and myocardial blood flow. It is tempting to invoke the/3-adrenergic properties of cardiac stimulation to explain the success of epinephrine. However, animal studies have demonstrated that all strong t~-adrenergic drugs (epinephrine, phenylephrine, methoxamine, dopamine, norepinephrine) are equally successful in aiding resuscitation regardless of the /3-adrenergic potency. /3-Adrenergic agonists without alpha activity (isoproterenol, dobutamine) are no better than
78 placebo, c~-Adrenergic blockade precludes resuscitation while /3-adrenergic blockade has no effect on the ability to restore spontaneous circulation. It is generally believed that the ability of epinephrine to increase the amplitude of ventricular fibrillation (a/3-adrenergic effect) makes defibrillation easier. In fact, animal studies have shown that epinephrine does not improve the success of or decrease the energy necessary for defibrillation. Retrospective clinical studies have shown no effect of epinephrine on defibrillation success. The/3-adrenergic effects of epinephrine are potentially deleterious during cardiac arrest. In the fibrillating heart, epinephrine increases myocardial oxygen consumption. Myocardial lactate production in the fibrillating heart is unchanged after epinephrine administration during CPR, suggesting that the increased coronary blood flow does not improve the oxygen supply to demand ratio. Large doses of epinephrine given during CPR increase deaths in swine early after resuscitation due to tachyarrhythmias and hypertension. In spite of these theoretical considerations, survival and neurologic outcome studies have shown no difference when epinephrine is compared with a pure a-agonist (methoxamine or phenylephrine) during CPR in animals or humans. Because of the long experience with epinephrine, it remains the vasopressor of choice in CPR. It should be administered whenever resuscitation has not occurred after adequate chest compressions and ventilation have been started and defibrillation attempted, if appropriate.
Epinephrine Dose When added to chest compressions, epinephrine helps develop the critical coronary perfusion pressure necessary to provide enough myocardial blood flow for restoration of spontaneous circulation. The standard dose used in animals and humans for many years has been 0.5 to 1.0 mg intravenously. On a weight basis, this dose is approximately 0.1 mg/kg in animals but only 0.015 mg/kg in humans. In some animal models, the standard dose of epinephrine (0.02 mg/kg) is insufficient to improve coronary perfusion pressure and blood flow, but a high dose (0.2 mg/kg) improves hemodynamics to levels compatible with successful resuscitation. Therefore, it has been suggested that higher doses of epinephrine in human CPR might improve myocardial and cerebral perfusion and improve success of resuscitation.
CHARLESW. 01-10 There are several case reports and a series of children (with historical controls) that demonstrated return of spontaneous circulation when large doses (0.1 to 0.2 mg/kg) of epinephrine were given to patients who had failed resuscitation with standard doses. Outcome studies prospectively comparing standard and high-dose epinephrine have not demonstrated conclusively that higher doses will improve survival. There are two randomized blinded studies of standard and high-dose epinephrine in a swine cardiac arrest model. There was no difference in 24-hour survival or neurologic outcome, but more of the high-dose animals died in the early postresuscitation period due to a hyperdynamic state. There are four published studies comparing standard doses (1 to 2 rag) to high doses (5 to 18 mg) of epinephrine in human CPR. All are prospective randomized double-blind clinical trials in cardiac arrest victims, primarily out-of-hospital. The resuits of two of the studies suggested there may be an improvement in immediate resuscitation with high-dose epinephrine while the other two found no difference. None of the studies found any improvement in survival to hospital discharge. High doses of epinephrine apparently are not needed as initial therapy for most cardiac arrests and potentially could be deleterious under some circumstances. However, the successful case reports were in patients with prolonged CPR and the high doses were given as "rescue" therapy when standard doses had failed. This may be the appropriate place for higher doses of epinephrine in CPR practice. Current recommendations are to give 1 mg intravenously every 3 to 5 minutes in the adult. If this dose seems ineffective, higher doses (3 to 8 rag) should be considered.
Sodium Bicarbonate Considerable concern has been expressed in recent years over the implications of gas transport physiology for acid-base homeostasis during CPR. Intravenous sodium bicarbonate combines with hydrogen ion resulting in the liberation of CO 2. The arterial Pco 2 is temporarily elevated until the excess CO 2 is eliminated through the lungs. It is only with the elimination of the volatile acid (CO2) that bicarbonate becomes an effective buffer. It has been suggested that sodium bicarbonate administration during CPR could be harmful, since tissue acidosis is primarily caused by the low blood flow
CARDIOPULMONARY RESUSCITATION:CURRENTSTATUS and accumulation of C O 2 in the tissues. C O 2 readily diffuses across cell membranes and the blood-brain barrier while bicarbonate diffuses much more slowly. Thus, it is possible that sodium bicarbonate administration could result in a "paradoxical" worsening of intracellular and cerebral acidosis by further raising intracellular and cerebral CO 2 without a balancing increase in bicarbonate. Direct evidence of this occurring during CPR is lacking at this time. Measurement of myocardial intracellular pH during sodium bicarbonate administration did not detect a worsening acidosis. Similarly, recent studies of cerebral spinal fluid pH found no change following administration of clinically relevant sodium bicarbonate doses. Therefore, paradoxical acidosis remains a concern primarily on theoretical grounds. The usefulness of sodium bicarbonate therapy during CPR also rests primarily on theoretical grounds. Acidosis lowers fibrillation threshold and impairs the physiologic response to catecholamines. There have been some recent reports that sodium bicarbonate administration may improve resuscitation from prolonged arrest without CPR in dogs. However, conclusive evidence that sodium bicarbonate improves survival will require additional studies. In contrast, hypernatremia, hyperosmolarity, and metabolic alkalosis are well-documented after CPR when sodium bicarbonate is used. These abnormalities are associated with a low resuscitation rate and poor survival. Therefore, current knowledge suggests that sodium bicarbonate should be used judiciously during CPR, restricting its use primarily to arrests associated with hyperkalemia, severe pre-existing metabolic acidosis, and tricyclic or phenobarbital overdose. It may be considered for use in protracted resuscitation attempts after other modalities have been instituted. If it is used, the risk of paradoxical acidosis can be reduced by giving the bicarbonate slowly rather than by rapid intravenous bolus.
Routes of Administration The preferred route of administration of all drugs during CPR is intravenous and the doses referred to in this report are for intravenous use. The most rapid and highest drug levels occur with administration into a central vein. Therefore, when a central venous catheter is available
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during a cardiac arrest, it should be used for drug therapy. However, peripheral intravenous administration also is effective. The antecubital or external jugular vein should be the site of first choice for starting an infusion during resuscitation because starting a central line usually necessitates stopping CPR. Sites in the upper extremity and neck are preferred because of the paucity of blood flow below the diaphragm during CPR. Drugs administered in the lower extremity may be extremely delayed or not reach the sites of action. Even in the upper extremity, drugs may require 1 to 2 minutes to reach the central circulation. Onset of action may be speeded if a drug bolus is followed by a 20- to 30-mL bolus of intravenous fluid. Epinephrine, lidocaine, and atropine do not injure the lungs and can be absorbed from the tracheal mucosa. Therefore, if intravenous access cannot be established, the endotracheal route provides an alternative for these drugs following intubation. Sodium bicarbonate should not be given by this route. The time to effect and drug levels achieved are very inconsistent using this route during CPR. Studies have demonstrated that volumes of 5 to 10 mL need to be delivered to have reasonable uptake. It is likely that higher doses of the drugs need to be used via this route; 2 to 2.5 times the intravenous dose is recommended currently. Studies conflict on whether deep injection is better than simple instillation in the tube.
REFERENCES 1. Berg RA, Kern KB, Sanders AB, et al: Bystander cardiopulmonary resuscitation. Is ventilation necessary? Circulation 88:1907-1915, 1993 2. Berg RA, Wilcoxson D, Hilwig RW, et al: The need for ventilatory support during bystander cardiopulmonary resuscitation. Ann Emerg Med 26:342-350, 1995 3. Berg RA, Kern KB, Hilwig RW, et al: Assisted ventilation does not improve outcome in a porcine model of single-rescuer bystander CPR. Circulation 95:1635-1641, 1997 4. Berg RA, Hilwig RW, Kern KB, et al: Assisted ventilation during "bystander" CPR improves outcome in a swine model of pediatric asphyxial cardiac arrest. Circulation 1999 (in press) 5. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closedchest cardiac massage. JAMA 173:1064-1067, 1960 6. Criley JM, Blaufuss AH, Kissel GL: Cough-induced cardiac compression. Self-administration form of cardiopulmonary resuscitation. JAMA 236:1246-1250, 1976 7. Sanders AB, Kern KB, Otto CW, et al: End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. A prognostic indicator for survival. JAMA 262:1347-1351, 1989
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8. Levine RL, Wayne MA, Miller CC: End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med 337:301-306, 1997 9. Redding JS, Pearson JW: Evaluation of drugs for cardiac resuscitation. Anesthesiology 24:203-207, 1963
SUGGESTED READING American Heart Association: Textbook of Advanced Cardiac Life Support. Dallas, TX, American Heart Association, 1994, pp 1-285 Emergency Cardiac Care Committee and Subcommittees, American Heart Association: Guidelines for cardiopulmonary
resuscitation and emergency cardiac care. JAMA 268:21712295, 1992 Otto CW: Cardiopuhnonary resuscitation, in Barash PG, Cullen BF, Stoelting RK (eds): Clinical Anesthesia (ed 3). Philadelphia, PA, Lippencott-Raven, 1997, pp 1389-1410 Otto CW: Cardiopulmonary resuscitation, in Longnecker DE, Tinker JH, Morgan GE (eds): Principles and Practice of Anesthesiology. St Louis, MO, Mosby-Yearbook, 1998, pp 647-679 Proceedings of the 1985 National Conference on Standards and Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiac Care. Montgomery WH (ed): Circulation Supplement 74:IV-l-IV-153, 1986 (suppl)