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Asynchronous and other alternative methods of ventilation during CPR
T h e Future The mechanism of blood flow engendered by closed-chest resuscitation techniques m a y not be as i m p o r t a n t as its goal: successful resuscitation and long-term functional survival. A number of recent studies indicate that resuscitation outcome will be determined by myocardial and cerebral perfusion produced by artificial circulatory techniques. Future investigations m u s t focus on clinically measurable variables in defining o p t i m a l closed-chest techniques. Closed-chest techniques for resuscitation, regardless of method1 seem superior to open massage, for t h e y m a y be p r a c t i c e d b y laymen and first rescuers. Twenty-four years of clinical experience supports the use of closed-chest CPR as a shortterm circulatory support technique. Future studies will address refinements in techniques to optimize o u t c o m e for the victim of cardiac arrest.
References 1. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closed-chest cardiac massage. JAMA 1960;173:1064-1067. 2. Benson DW, Jude JR, Kouwenhoven WB: External cardiac massage. Anesth Analg 1963;42:75-83. 3. Safar P, Brown TC, Holtey WJ: Failure of closed chest massage to produce pulmonary ventilation. Dis Chest 1962;41:1-8. 4. Safar P, Brown TC, Holtey WJ, et al: Ventilation and circulation with closed-chest cardiac massage in man. JAMA 1961;176: 574-576. 5. Redding JS, Pearson JW: Resuscitation from asphyxia. JAMA 1962;182:283-286. 6. Redding JS, Pearson JW: Evaluation of drugs for cardiac resuscitation. Anesthesiology 1963;24:203-207. 7. Weale FE, Rothwell-Jackson RL: The efficiency of cardiac massage. Lancet 1962;1:990-992. 8. MacKenzie GJ, Taylor SH, McDonald AH, et ah Haemodynamic effects of external cardiac compression. Lancet 1964;1:13421345. 9. Gall F: Incompetence of the atrioventricular valves during cardiac massage. J Cardiovasc Surg 1965;6:356-360.
10. Thomsen JE, Stenlund RR, Rowe GG: Intracardiac pressures during closed-chest cardiac massage. JAMA 1968;205:46-48. 11. Criley JM, Blaufuss AH, Kissel GL: Cough-induced cardiac compression. Self-administered form of cardiopulmonary resuscitation. JAMA 1976;236:1246-1250. 12. Rudikoff MT, Maughan WL, Effron M, et ah Mechanisms of blood flow during cardiopulmonary resuscitation. Circulation 1980;61:345-352. 13. Niemann JT, Rosborough JE Hausknecht M, et ah Pressuresynchronized cineangiography during experimental cardiopulmonary resuscitation. Circulation 1981;64:985-991. 14. Chandra N, Weisfeldt ML, Tsitlik J, et ah Augmentation of carotid flow during cardiopulmonary resuscitation by ventilation at high airway pressure simultaneous with chest compression. Am J Cardiol 1981;48:1053-1063. 15. Criley JM, Niemann JT, Rosborough JP, et al: The heart is a conduit in CPR. Crit Care Med 1981;9:373-374. 16. Fisher J, Vaghaiwalla F, Tsitlik J, et ah Determinants and clinical significance of jugular venous valve competence. Circulation 1982;65:188-196. 17. Rich S, Wix HL, Shapiro El?: Clinical assessment of heart chamber size and valve motion during cardiopulmonary resuscitation by two-dimensional echocardiography. Am Heart J 1981;102:368-373. 18. Werner JA, Greene HL, Janko CL, et ah Visualization of cardiac valve motion in man during external chest compression using two-dimensional echocardiography. Implications regarding the mechanism of flow. Circulation 1981;63:1417-1421. 19. Hodgkin BC, Burkett DE, Babbs CF, et ah Blood pressure and flow with thoracic venting during cardiopulmonary resuscitation, abstract. Circulation 1980;62(suppl III):III-339. 20. Redding JS, Jaynes RR, Thomas JD: "Old" and "new" CPR manually performed in dogs. Crit Care Med 1981;9:386-387. 21. Babbs CF, Tacker WA, Paris RL, et ah CPR with simultaneous compression and ventilation at high airway pressure in 4 animal models. Crit Care Med 1982;10:501-504. 22. Babbs CF: New versus old theories of blood flow during CPR. Crit Care Med 1980;8:191-195.
Asynchronous and Other Alternative Methods of Ventilation During CPR Richard J Melker, MD / Gainesville, Florida
Current standards for ventilation during cardiopulmonary resuscitation are not supported by recent and ongoing investigations. This is particularly true in victims with an unprotected airway. Currently used flow rates and inFrom the Departments of Anesthesiology, Pediatrics, and Surgery, University of Florida College of Medicine, Gainesville, Florida. Address for reprints: Richard J Melker, MD, Department of Anesthesiology, Box J-254, J Hillis Miller Health Center, Gainesville, Florida 32610. 13:9 September 1984 (Part 2)
spiratory times predispose to gastric insufflation and its complications. Potential changes and corrections that m a y benefit the victim of cardiac arrest are reviewed. [Melker RJ: Asynchronous and other alternative methods of ventilation during CPR. Ann Emerg Med September 1984 (Part 2);13:758-761. Key words: cardiopulmonary resuscitation; ventilation.]
Introduction Current standards for ventilation during cardiopulmonary
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resuscitation (CPR) recommend that a 0.8 to 1.2 L tidal volume (VT) be interposed in 0.5 seconds after every fifth chest compression.I,2 As early as 1963 Safar recognized the risks associated with this practice, stating, "With bag-mask or mouth-to-mouth ventilation, it is almost impossible to inflate the lungs adequately in less than one second. Very high inflation pressures would be required, which in the non-intubated subject, would lead to gastric insufflation or may be impossible because of air leaks at the subject's face. "3 Ruben et af4 demonstrated that the airway pressure producing gastric insuffiation during face mask ventilation averaged 19 cm H20. Omato et als reported peak inflation pressures (PIP) of 43 _ 8 cm H20 and lung compliances (CL) of 0.022 + 0.02 L/cm H20 (normal C L > 0.1 L/cm H20 ) in intubated patients during CPR with an inspiratory time (TI) of 1.0 second and a VT of at least 10 cc/kg. These findings suggest that gastric insufflation may be a major hazard of CPR in victims with an unprotected airway. Few data exist regarding the incidence of gastric distention, regurgitation, and pulmonary aspiration during CPR, nor are there data that indicate whether the risk is greater with one rescuer or with two. Nagel et al 6 studied complications of CPR in 2,228 cases of prehospital cardiac arrest that came to autopsy. Gastric dilatation was found in 28% of the cases, oropharyngeal vomitus in 9.5%, tracheal vomitus in 8.9%, and aspiration vomitus in 11.3%. The percentage of patients who were ventilated with an unprotected airway is unknown. Bjork et a17 studied 63 survivors of cardiopulmonary arrest occurring both in and out of the hospital. Thirty-five percent were found to have aspiration, and p n e u m o n i a occurring in the i m m e d i a t e postresuscitation period was significantly related to mortality. An obvieus question that has not been addressed is whether the complications resulting from basic cardiac life support-CPR (BCLS-CPR) are outweighed by the improved survival from its application. Numerous animal studies have demonstrated marginal cerebral and minimal coronary blood flow with BCLS-CPR.S,9 Improved BCLS-CPR techniques that would reduce the risk of complications and/or improve cerebral and coronary blood flow, however, should still be sought. Reviewed are alternative CPR sequences that might be used in victims with an unprotected airway.
Single-Rescuer BCLS-CPR Single-rescuer standards for ventilation are imprecise. It is recommended that "two very quick," "flaW' breaths be delivered in four to five seconds after external cardiac compression (ECC).I,2 No parameters for TI, sequencing, or VT are given. When training with a CPR manikin, a single rescuer is taught to deliver, in a stair-step manner, a first breath of 0.8 L and a second so that the two breaths total 2.0 L.2 In 1981 our investigation group demonstrated that the pattern recommended during manikin training requires breaths of both unequal T I and unequal VT.10 The ability to deliver these breaths in a stair-step manner was shown to be largely an artifact of the valving system of the manikin. Using both a 75-kg swine and a test lung, we showed that the majority of the first breath is exhaled before the second breath can be delivered, and that the second breath is approximately twice the VT of the first. The large VT of the second breath produced extremely high airway pressures (greater than 80 cm H20 ) and peak inspiratory flows (greater than 200 L/min). We suggested that this pattern of ventilation would lead to massive gastric insufflation in human beings with an unprotected airway. Using a mechanical 10/759
model to simulate the tracheo-bronchial tube, esophagus, and the stomach, we demonstrated that half the second breath would enter the stomach when C L was normaf.n With the C L reported by Omato during CPR, 75% of the delivered gas entered the stomach. We therefore recommended that a single breath with a longer T I replace the two stair-step breaths currently advocated. Further study is necessary to define the parameters of ventilation that will optimize lung inflation without adversely affecting blood flow and still allow the pauses that are necessary for ventilation and ECC with a single rescuer.
Two-Rescuer BCLS-CPR If short T I produce high airway flows and high PIP which cause gastric insufflation, then one way to reduce this risk would be to lengthen the T I. This can be accomplished by two methods. First, the rate of ECC could be reduced. Halving the rate of ECC from 60 to 30 per minute would double the time for ventilation if the duration of compression remains constant. Taylor et a112 showed that at compression rates of 40, 60, and 80 per minute, carotid arterial flow index (Doppler technique) did not change if a constant compression duration of 60% was maintained for each cycle. 12 The effects of rates slower than 40 per minute during BCLSCPR have not been studied. A second strategy would be to increase the T I by pausing after every fifth ECC. At the rate of 60 compressions per minute, the total number of compressions would be reduced to 48 per minute if the T I were increased to 1.5 seconds. Even if the T I is increased, an additional problem may arise. Using the mechanical lung and stomach model we demonstrated that a" longer T I will increase lung inflation and reduce gastric insuffiation. 13 These effects are greatest at normal CL, however, and greatly diminish at the C L values reported by Omato. s At normal Cv increasing the T I from 0.5 seconds to 1.5 seconds reduced gastric gas and thus increased lung inflation by 0.2 L with a VT of 0.8 L. At a C L of 0.02 L/cm H20 , increasing the T I from 0.5 to 1.5 seconds increased lung inflation by only 0.05 L. Omato et al measured C L 35 -+ 16 minutes after cardiac arrest. If changes in C e develop slowly after cardiac arrest or can be attenuated by adequate lung inflation, then increasing T I would be beneficial. If C L decreases rapidly after arrest, however, then increasing T I may be of little value.
Asynchronous Ventilation-CPR Rudikoff et a114 demonstrated a significant increase in common carotid arterial blood flow during the chest compression immediately following ventilation. 14 They postulated that this improvement in flow is a resuk of the higher intrathoracic pressure caused by positive pressure ventilation. Subsequent studies using techniques designed to increase intrathoracic pressure have, in fact, demonstrated improved cerebral and coronary blood flow. These techniques usually involve simultaneous chest compression and ventilation (SCV-CPR) and have been combined with abdominal binding or simultaneous abdominal compression.S,lS, 16 The latter has improved not only coronary blood flow, but also survival in dogs. These are all advanced cardiac life support techniques that require endotracheal intubation. Can these techniques be exploited in cardiac arrest victims prior to intubation? Ventilation with an unprotected airway can be performed by two techniques. In the first, mouth-to-mouth is used. In the second, a mechanical ventilation device (ie, bag-valve-mask
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or oxygen-powered breathing device) replaces mouth-tomouth ventilation. With either technique it is possible to deliver breaths with a long T I asynchronous with ECC (asynchronous ventilation CPR, ASV-CPR). ASV-CPR has two theoretical advantages over BCLS-CPR: 1) if VT is constant, the longer T I will reduce the risk of gastric insufflation; and 2} a portion of each ventilation will occur simultaneous with ECC. If an adequate mask-to-face seal can be maintained, then intrathoracic pressure will rise more when ventilation is simultaneous with compression than when ventilation is between compressions. Thus ASV-CPR combines some of the benefits of SCV-CPR while still maintaining lower PIP between compressions. One might intuitively be concerned that during simultaneous ventilation and compression, high PIP would provoke gastric insufflation. During ECC, however, pressure rises equally in all intrathoracic structures; therefore, intrapulmonary and intraesophageal pressures will rise equally to a level greater than the esophageal opening pressure, and gastric insufflation will be prevented. While ventilation might not occur during this period, it would occur during the portion of ventilation between compressions. We have compared BCLS-CPR to ASV-CPR in swine with a protected airway. 17 Airway pressure between chest compressions was significantly lower when using ASV-CPR (ASV-CPR, 24.2 m m Hg; BCLS-CPR, 34.9 m m Hg). Arterial and venous blood gases were similar. During ASV-CPR, T I averaged 1.6 seconds, and the flow rate was 40 L/min; during BCLS-CPR, T I was 0.5 seconds and flow rates averaged 120 L/min. ASV-CPR produced significantly higher common carotid artery blood flow when applied after BCLSCPR; however, when ASV-CPR was applied first, there was no change in flow. These results do not indicate which technique would be better when applied alone. Further studies are necessary to determine whether ASV-CPR would reduce the risk of gastric insuffiation and improve cerebral and coronary blood flow with an unprotected airway. Another technique that might reduce the risk of gastric instffflation has long been available. In 1961 Sellick 18 demonstrated that cricoid pressure could prevent gastric regurgitation during induction of anesthesia. He also suggested using the maneuver to prevent inflation of the stomach during mouth-to-mouth or bag-mask ventilation. A subsequent study by Salem et all9 has shown the efficacy of cricoid pressure in preventing gastric inflation during bag-mask ventilation in children. This technique, combined with CPR, could reduce significantly the risk of gastric insuffiation. Conclusions
Survival from out-of-hospital cardiac arrest in the absence of rapid availability of advanced cardiac life support is rare. No study has addressed the question of whether the complications of BCLS-CPR make its application inappropriate in settings in which advanced life support is readily available. Animal studies demonstrate that BCLS-CPR techniques provide little cerebral or coronary blood flow. Newer techniques, including SCV-CPR with synchronized abdominal compression, markedly improve flow and survival. These advanced techniques that require endotracheal intubation are still experimental. We have addressed possible changes in CPR standards in the BCLS setting, where victims have an unprotected airway. Increasing T I has been suggested as a method of reduc13:9 September 1984 (Part 2)
mg the risk of gastric insuffiation. Performing ventilation asynchronous with chest compression may provide additional benefit, as seen with SCV-CPR in which a portion of each ventilation occurs during compression. These techniques have theoretical advantages over BCLS-CPR, but only one study has demonstrated this. Additional data supporting change must be available before new recommendations can be promulgated. One of the greatest challenges in prehospital cardiac arrest is to improve BCLS-CPR techniques as a temporizing measure until the arrival of advanced life support. References
1. American Heart Association: Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). ]AMA 1980;244:462-468. 2. A Manual for Instructors of Basic Life Support. Dallas, American Heart Association, 1980, p 47, 81. 3. Safar P (ed): An International Symposium on Resuscitation: Controversial Aspects. Heidelberg, Springer-Verlag, 1963, p 27. 4. Ruben H, Knudsen EJ, Carugati G: Gastric inflation in relation to airway pressure. Acta Anaesthesiol Scand 1961;5:107-114. 5. Ornato lP, Bryson BL, Donovan PJ, et ah Measurement of ventilation during cardiopulmonary resuscitation. Crit Care Med 1983;1:79-82.
6. Nagel EL, Fine EG, Krischer JP, et ah Complications of CPR, abstract. Crit Care Med 1981;9:424. 7. Bjork RJ, Snyder BD, Campion BC, et ah Medical complications of cardiopulmonary arrest. Arch Intern Med 1982;142:500503. 8. Koehler RC, Chandra N, Guerci AD, et ah Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs. Circulation 1983;67:266-275.
9. Ditchey RV, Winkler JV, Rhodes CA: Relative lack of coronary blood flow during closed-chest resuscitation in dogs. Circulation 1982;66:297-302.
10. Nielker R, Cavallaro D, Krischer 1: One-rescuer CPR: A reappraisal of present recommendations for ventilation, abstract. Crit Care Med 1981;9:423. 11. Nielker RJ, Banner MI: Ventilation during cardiopulmonary resuscitation: One-rescuer standards reappraised, abstract. Anesthesiology, to be published. 12. Taylor GJ, Tucker WNI, Greene HL: Importance of prolonged compression during cardiopulmonary resuscitation in man. N Engl ] Med 1977;296:1515-1517.
13. Nielker RI, Banner Nil: Ventilation during cardiopulmonary resuscitation: Two-rescuer standards reappraised, abstract. Ann Emerg Med 1984;13:403-404. 14. Rudikoff NIT, Nianghan WL, Effron NI, et ah Mechanisms of blood flow during cardiopulmonary resuscitation. Circulation 1980;61:345-352. 15. Chandra N, Weisfeldt WL, Tsitlik l, et al: Augmentation of carotid flow during cardiopulmonary resuscitation by ventilation at high airway pressure simultaneous with chest compression. Am [ Cardiol 1981;48:1053-1063. 16. Niemann J, Rosborough J, Criley l: Coronary perfusion pressure during cardiopulmonary resuscitation: A determinant of successful defibrillation, abstract..Clin Res 1983;3h208A. 17. Melker Rl, Cavallaro DL: Synchronous and asynchronous ventilation during cardiopulmonary resuscitation, abstract. Arm Emerg Med 1983;12:142.
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18. Sellick BA: Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet 1961;2:404406.
19. Salem MR, Wong AY, Mani M: Efficacy of cricoid pressure in preventing gastric inflation during bag-mask ventilation in pediatric patients. Anesthesiology 1974;40:96-98.
Preclinical Studies of Abdominal Counterpulsation in CPR Charles F Babbs, MD, PhD / West Lafayette, Indiana
Abdominal counterpulsation added to standard cardiopulmonary resuscitation improves blood flow in animal models when compared to chest compressions alone. Similar effects can be demonstrated in analog and digital computer models of the circulation. The technique generates both central aortic and central venous pressure pulses, and successful application of the method depends on maximizing the former and minimizing the latter. Proper technique is important in order to generate the largest possible arteriovenous pressure difference. [Babbs CF: Preclinical studies of abdominal counterpulsation in CPR. Ann Emerg Med September 1984 (Part 2);13:761-763. Key words: abdominal counterpulsation; cardiopulmonary resuscitation.]
Introduction The technique of abdominal counterpulsation during cardiopulmonary resuscitation (CPR) consists of applying external pressure to the abdomen during "diastole," the chest relaxation phase. During interposed abdominal compression-CPR (IAC-CPR), abdominal pressure is maintained manually over the midabdomen for 50% of cycle time, exactly 180 degrees out of phase with chest Compressions. A folded blood pressure cuff placed between the hands and the abdomen and connected to an aneroid manometer may be used to monitor the pressure applied. We have obtained good results with negligible trauma in animals using applied abdominal pressures of 120 to 150 m m Hg.
Hemodynamic Effects in the Canine Arrest Model The hemodynamic effects of abdominal counterpulsation have been discovered independently by several research teams in the last decade. In 1976 Ohomoto and coworkers 1 at Tokyo Women's Medical College described an arrangement of two mechanical pistons, one that compressed the chest and another that compressed the abdomen. They termed the technique "counter-massage," and found in preliminary studies that phased abdominal compression for 80% of cycle time and chest compression for 25% of cycle time appeared to improve carotid flow, mean aortic presFrom the Biomedical Engineering Center, Purdue University, West Lafayette, indiana. Address for reprints: Charles F Babbs, MD, PhD, Biomedical Engineering Center, AA Potter Building, Room 204, Purdue University, West Lafayette, indiana 47907. Supported by Research Career Development Award HL-00587 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. 12/761
sure, and short-term survival in anesthetized dogs with ventAcular fibrillation. Rosborough and coworkers 2 in Houston, while attempting to mimic the physiology of "cough-CPR" in an animal model, 3 combined simultaneous high-pressure lung inflation with abdominal compression. They found that abdominal compression and ventilation alone could maintain carotid flow and aortic blood pressure during ventricular fibrillation in dogs, and they suggested the technique as a new CPR modality. In 1981 Ralston, of Purdue University, observed the hemodynamic effects of interposed abdominal compressions as an adjunct to mechanical chest compression in dogs. 4 Interposed abdominal compressions dramatically improved brachial artery blood pressure without a comparable increase in central venous pressure {Figure 1). A subsequent controlled study of IAC-CPR in ten dogs with electrically induced fibrillation showed that the technique significantly improved cardiac output and diastolic arterial pressures. 4 In this study cardiac output was measured with an indicator dilution method specially modified for CPR, s and constant pressure {20 cm H20 ) ventilation was used. Voorhees et al6 at Purdue have continued this line of research and have shown an approximate doubling of cardiac output, diastolic arterial pressure, and diastolic arteriovenous pressure difference, with significant improvement in total body oxygen deliver~, when IAC was added to otherwise standard CPR {Figure 2). In this second study a specially modified spirometer recorded oxygen consumption during CPR. Cardiac output was measured by the Fick technique (0 2 consumption/A-V O 2 difference), and constant volume rather than constant pressure ventilation was applied. At about the same time Coletti and coworkers in New York were studying the influence of abdominal counterpulsation on cerebral and coronary blood flow in a canine model of cardiogenic shock.e,8 They found that when manual abdominal compressions were interposed between heartbeats (as judged from the ECG trace}, both carotid and coronary flow, measured with implanted electromagnetic probes, increased. The recent study by Walker and coworkers in Detroit 9 has confirmed the earlier animal experiments. These investigators measured perfusion of the cerebral cortex during IAC versus standard CPR in a canine model. They used both manual chest and manual abdominal compression in
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References 1. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closed-chest cardiac massage. JAMA 1960;173:1064-1067. 2. Benson DW, Jude JR, Kouwenhoven WB: External cardiac massage. Anesth Analg 1963;42:75-83. 3. Safar P, Brown TC, Holtey WJ: Failure of closed chest massage to produce pulmonary ventilation. Dis Chest 1962;41:1-8. 4. Safar P, Brown TC, Holtey WJ, et al: Ventilation and circulation with closed-chest cardiac massage in man. JAMA 1961;176: 574-576. 5. Redding JS, Pearson JW: Resuscitation from asphyxia. JAMA 1962;182:283-286. 6. Redding JS, Pearson JW: Evaluation of drugs for cardiac resuscitation. Anesthesiology 1963;24:203-207. 7. Weale FE, Rothwell-Jackson RL: The efficiency of cardiac massage. Lancet 1962;1:990-992. 8. MacKenzie GJ, Taylor SH, McDonald AH, et ah Haemodynamic effects of external cardiac compression. Lancet 1964;1:13421345. 9. Gall F: Incompetence of the atrioventricular valves during cardiac massage. J Cardiovasc Surg 1965;6:356-360.
10. Thomsen JE, Stenlund RR, Rowe GG: Intracardiac pressures during closed-chest cardiac massage. JAMA 1968;205:46-48. 11. Criley JM, Blaufuss AH, Kissel GL: Cough-induced cardiac compression. Self-administered form of cardiopulmonary resuscitation. JAMA 1976;236:1246-1250. 12. Rudikoff MT, Maughan WL, Effron M, et ah Mechanisms of blood flow during cardiopulmonary resuscitation. Circulation 1980;61:345-352. 13. Niemann JT, Rosborough JE Hausknecht M, et ah Pressuresynchronized cineangiography during experimental cardiopulmonary resuscitation. Circulation 1981;64:985-991. 14. Chandra N, Weisfeldt ML, Tsitlik J, et ah Augmentation of carotid flow during cardiopulmonary resuscitation by ventilation at high airway pressure simultaneous with chest compression. Am J Cardiol 1981;48:1053-1063. 15. Criley JM, Niemann JT, Rosborough JP, et al: The heart is a conduit in CPR. Crit Care Med 1981;9:373-374. 16. Fisher J, Vaghaiwalla F, Tsitlik J, et ah Determinants and clinical significance of jugular venous valve competence. Circulation 1982;65:188-196. 17. Rich S, Wix HL, Shapiro El?: Clinical assessment of heart chamber size and valve motion during cardiopulmonary resuscitation by two-dimensional echocardiography. Am Heart J 1981;102:368-373. 18. Werner JA, Greene HL, Janko CL, et ah Visualization of cardiac valve motion in man during external chest compression using two-dimensional echocardiography. Implications regarding the mechanism of flow. Circulation 1981;63:1417-1421. 19. Hodgkin BC, Burkett DE, Babbs CF, et ah Blood pressure and flow with thoracic venting during cardiopulmonary resuscitation, abstract. Circulation 1980;62(suppl III):III-339. 20. Redding JS, Jaynes RR, Thomas JD: "Old" and "new" CPR manually performed in dogs. Crit Care Med 1981;9:386-387. 21. Babbs CF, Tacker WA, Paris RL, et ah CPR with simultaneous compression and ventilation at high airway pressure in 4 animal models. Crit Care Med 1982;10:501-504. 22. Babbs CF: New versus old theories of blood flow during CPR. Crit Care Med 1980;8:191-195.
Asynchronous and Other Alternative Methods of Ventilation During CPR Richard J Melker, MD / Gainesville, Florida
Current standards for ventilation during cardiopulmonary resuscitation are not supported by recent and ongoing investigations. This is particularly true in victims with an unprotected airway. Currently used flow rates and inFrom the Departments of Anesthesiology, Pediatrics, and Surgery, University of Florida College of Medicine, Gainesville, Florida. Address for reprints: Richard J Melker, MD, Department of Anesthesiology, Box J-254, J Hillis Miller Health Center, Gainesville, Florida 32610. 13:9 September 1984 (Part 2)
spiratory times predispose to gastric insufflation and its complications. Potential changes and corrections that m a y benefit the victim of cardiac arrest are reviewed. [Melker RJ: Asynchronous and other alternative methods of ventilation during CPR. Ann Emerg Med September 1984 (Part 2);13:758-761. Key words: cardiopulmonary resuscitation; ventilation.]
Introduction Current standards for ventilation during cardiopulmonary
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resuscitation (CPR) recommend that a 0.8 to 1.2 L tidal volume (VT) be interposed in 0.5 seconds after every fifth chest compression.I,2 As early as 1963 Safar recognized the risks associated with this practice, stating, "With bag-mask or mouth-to-mouth ventilation, it is almost impossible to inflate the lungs adequately in less than one second. Very high inflation pressures would be required, which in the non-intubated subject, would lead to gastric insufflation or may be impossible because of air leaks at the subject's face. "3 Ruben et af4 demonstrated that the airway pressure producing gastric insuffiation during face mask ventilation averaged 19 cm H20. Omato et als reported peak inflation pressures (PIP) of 43 _ 8 cm H20 and lung compliances (CL) of 0.022 + 0.02 L/cm H20 (normal C L > 0.1 L/cm H20 ) in intubated patients during CPR with an inspiratory time (TI) of 1.0 second and a VT of at least 10 cc/kg. These findings suggest that gastric insufflation may be a major hazard of CPR in victims with an unprotected airway. Few data exist regarding the incidence of gastric distention, regurgitation, and pulmonary aspiration during CPR, nor are there data that indicate whether the risk is greater with one rescuer or with two. Nagel et al 6 studied complications of CPR in 2,228 cases of prehospital cardiac arrest that came to autopsy. Gastric dilatation was found in 28% of the cases, oropharyngeal vomitus in 9.5%, tracheal vomitus in 8.9%, and aspiration vomitus in 11.3%. The percentage of patients who were ventilated with an unprotected airway is unknown. Bjork et a17 studied 63 survivors of cardiopulmonary arrest occurring both in and out of the hospital. Thirty-five percent were found to have aspiration, and p n e u m o n i a occurring in the i m m e d i a t e postresuscitation period was significantly related to mortality. An obvieus question that has not been addressed is whether the complications resulting from basic cardiac life support-CPR (BCLS-CPR) are outweighed by the improved survival from its application. Numerous animal studies have demonstrated marginal cerebral and minimal coronary blood flow with BCLS-CPR.S,9 Improved BCLS-CPR techniques that would reduce the risk of complications and/or improve cerebral and coronary blood flow, however, should still be sought. Reviewed are alternative CPR sequences that might be used in victims with an unprotected airway.
Single-Rescuer BCLS-CPR Single-rescuer standards for ventilation are imprecise. It is recommended that "two very quick," "flaW' breaths be delivered in four to five seconds after external cardiac compression (ECC).I,2 No parameters for TI, sequencing, or VT are given. When training with a CPR manikin, a single rescuer is taught to deliver, in a stair-step manner, a first breath of 0.8 L and a second so that the two breaths total 2.0 L.2 In 1981 our investigation group demonstrated that the pattern recommended during manikin training requires breaths of both unequal T I and unequal VT.10 The ability to deliver these breaths in a stair-step manner was shown to be largely an artifact of the valving system of the manikin. Using both a 75-kg swine and a test lung, we showed that the majority of the first breath is exhaled before the second breath can be delivered, and that the second breath is approximately twice the VT of the first. The large VT of the second breath produced extremely high airway pressures (greater than 80 cm H20 ) and peak inspiratory flows (greater than 200 L/min). We suggested that this pattern of ventilation would lead to massive gastric insufflation in human beings with an unprotected airway. Using a mechanical 10/759
model to simulate the tracheo-bronchial tube, esophagus, and the stomach, we demonstrated that half the second breath would enter the stomach when C L was normaf.n With the C L reported by Omato during CPR, 75% of the delivered gas entered the stomach. We therefore recommended that a single breath with a longer T I replace the two stair-step breaths currently advocated. Further study is necessary to define the parameters of ventilation that will optimize lung inflation without adversely affecting blood flow and still allow the pauses that are necessary for ventilation and ECC with a single rescuer.
Two-Rescuer BCLS-CPR If short T I produce high airway flows and high PIP which cause gastric insufflation, then one way to reduce this risk would be to lengthen the T I. This can be accomplished by two methods. First, the rate of ECC could be reduced. Halving the rate of ECC from 60 to 30 per minute would double the time for ventilation if the duration of compression remains constant. Taylor et a112 showed that at compression rates of 40, 60, and 80 per minute, carotid arterial flow index (Doppler technique) did not change if a constant compression duration of 60% was maintained for each cycle. 12 The effects of rates slower than 40 per minute during BCLSCPR have not been studied. A second strategy would be to increase the T I by pausing after every fifth ECC. At the rate of 60 compressions per minute, the total number of compressions would be reduced to 48 per minute if the T I were increased to 1.5 seconds. Even if the T I is increased, an additional problem may arise. Using the mechanical lung and stomach model we demonstrated that a" longer T I will increase lung inflation and reduce gastric insuffiation. 13 These effects are greatest at normal CL, however, and greatly diminish at the C L values reported by Omato. s At normal Cv increasing the T I from 0.5 seconds to 1.5 seconds reduced gastric gas and thus increased lung inflation by 0.2 L with a VT of 0.8 L. At a C L of 0.02 L/cm H20 , increasing the T I from 0.5 to 1.5 seconds increased lung inflation by only 0.05 L. Omato et al measured C L 35 -+ 16 minutes after cardiac arrest. If changes in C e develop slowly after cardiac arrest or can be attenuated by adequate lung inflation, then increasing T I would be beneficial. If C L decreases rapidly after arrest, however, then increasing T I may be of little value.
Asynchronous Ventilation-CPR Rudikoff et a114 demonstrated a significant increase in common carotid arterial blood flow during the chest compression immediately following ventilation. 14 They postulated that this improvement in flow is a resuk of the higher intrathoracic pressure caused by positive pressure ventilation. Subsequent studies using techniques designed to increase intrathoracic pressure have, in fact, demonstrated improved cerebral and coronary blood flow. These techniques usually involve simultaneous chest compression and ventilation (SCV-CPR) and have been combined with abdominal binding or simultaneous abdominal compression.S,lS, 16 The latter has improved not only coronary blood flow, but also survival in dogs. These are all advanced cardiac life support techniques that require endotracheal intubation. Can these techniques be exploited in cardiac arrest victims prior to intubation? Ventilation with an unprotected airway can be performed by two techniques. In the first, mouth-to-mouth is used. In the second, a mechanical ventilation device (ie, bag-valve-mask
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or oxygen-powered breathing device) replaces mouth-tomouth ventilation. With either technique it is possible to deliver breaths with a long T I asynchronous with ECC (asynchronous ventilation CPR, ASV-CPR). ASV-CPR has two theoretical advantages over BCLS-CPR: 1) if VT is constant, the longer T I will reduce the risk of gastric insufflation; and 2} a portion of each ventilation will occur simultaneous with ECC. If an adequate mask-to-face seal can be maintained, then intrathoracic pressure will rise more when ventilation is simultaneous with compression than when ventilation is between compressions. Thus ASV-CPR combines some of the benefits of SCV-CPR while still maintaining lower PIP between compressions. One might intuitively be concerned that during simultaneous ventilation and compression, high PIP would provoke gastric insufflation. During ECC, however, pressure rises equally in all intrathoracic structures; therefore, intrapulmonary and intraesophageal pressures will rise equally to a level greater than the esophageal opening pressure, and gastric insufflation will be prevented. While ventilation might not occur during this period, it would occur during the portion of ventilation between compressions. We have compared BCLS-CPR to ASV-CPR in swine with a protected airway. 17 Airway pressure between chest compressions was significantly lower when using ASV-CPR (ASV-CPR, 24.2 m m Hg; BCLS-CPR, 34.9 m m Hg). Arterial and venous blood gases were similar. During ASV-CPR, T I averaged 1.6 seconds, and the flow rate was 40 L/min; during BCLS-CPR, T I was 0.5 seconds and flow rates averaged 120 L/min. ASV-CPR produced significantly higher common carotid artery blood flow when applied after BCLSCPR; however, when ASV-CPR was applied first, there was no change in flow. These results do not indicate which technique would be better when applied alone. Further studies are necessary to determine whether ASV-CPR would reduce the risk of gastric insuffiation and improve cerebral and coronary blood flow with an unprotected airway. Another technique that might reduce the risk of gastric instffflation has long been available. In 1961 Sellick 18 demonstrated that cricoid pressure could prevent gastric regurgitation during induction of anesthesia. He also suggested using the maneuver to prevent inflation of the stomach during mouth-to-mouth or bag-mask ventilation. A subsequent study by Salem et all9 has shown the efficacy of cricoid pressure in preventing gastric inflation during bag-mask ventilation in children. This technique, combined with CPR, could reduce significantly the risk of gastric insuffiation. Conclusions
Survival from out-of-hospital cardiac arrest in the absence of rapid availability of advanced cardiac life support is rare. No study has addressed the question of whether the complications of BCLS-CPR make its application inappropriate in settings in which advanced life support is readily available. Animal studies demonstrate that BCLS-CPR techniques provide little cerebral or coronary blood flow. Newer techniques, including SCV-CPR with synchronized abdominal compression, markedly improve flow and survival. These advanced techniques that require endotracheal intubation are still experimental. We have addressed possible changes in CPR standards in the BCLS setting, where victims have an unprotected airway. Increasing T I has been suggested as a method of reduc13:9 September 1984 (Part 2)
mg the risk of gastric insuffiation. Performing ventilation asynchronous with chest compression may provide additional benefit, as seen with SCV-CPR in which a portion of each ventilation occurs during compression. These techniques have theoretical advantages over BCLS-CPR, but only one study has demonstrated this. Additional data supporting change must be available before new recommendations can be promulgated. One of the greatest challenges in prehospital cardiac arrest is to improve BCLS-CPR techniques as a temporizing measure until the arrival of advanced life support. References
1. American Heart Association: Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). ]AMA 1980;244:462-468. 2. A Manual for Instructors of Basic Life Support. Dallas, American Heart Association, 1980, p 47, 81. 3. Safar P (ed): An International Symposium on Resuscitation: Controversial Aspects. Heidelberg, Springer-Verlag, 1963, p 27. 4. Ruben H, Knudsen EJ, Carugati G: Gastric inflation in relation to airway pressure. Acta Anaesthesiol Scand 1961;5:107-114. 5. Ornato lP, Bryson BL, Donovan PJ, et ah Measurement of ventilation during cardiopulmonary resuscitation. Crit Care Med 1983;1:79-82.
6. Nagel EL, Fine EG, Krischer JP, et ah Complications of CPR, abstract. Crit Care Med 1981;9:424. 7. Bjork RJ, Snyder BD, Campion BC, et ah Medical complications of cardiopulmonary arrest. Arch Intern Med 1982;142:500503. 8. Koehler RC, Chandra N, Guerci AD, et ah Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs. Circulation 1983;67:266-275.
9. Ditchey RV, Winkler JV, Rhodes CA: Relative lack of coronary blood flow during closed-chest resuscitation in dogs. Circulation 1982;66:297-302.
10. Nielker R, Cavallaro D, Krischer 1: One-rescuer CPR: A reappraisal of present recommendations for ventilation, abstract. Crit Care Med 1981;9:423. 11. Nielker RJ, Banner MI: Ventilation during cardiopulmonary resuscitation: One-rescuer standards reappraised, abstract. Anesthesiology, to be published. 12. Taylor GJ, Tucker WNI, Greene HL: Importance of prolonged compression during cardiopulmonary resuscitation in man. N Engl ] Med 1977;296:1515-1517.
13. Nielker RI, Banner Nil: Ventilation during cardiopulmonary resuscitation: Two-rescuer standards reappraised, abstract. Ann Emerg Med 1984;13:403-404. 14. Rudikoff NIT, Nianghan WL, Effron NI, et ah Mechanisms of blood flow during cardiopulmonary resuscitation. Circulation 1980;61:345-352. 15. Chandra N, Weisfeldt WL, Tsitlik l, et al: Augmentation of carotid flow during cardiopulmonary resuscitation by ventilation at high airway pressure simultaneous with chest compression. Am [ Cardiol 1981;48:1053-1063. 16. Niemann J, Rosborough J, Criley l: Coronary perfusion pressure during cardiopulmonary resuscitation: A determinant of successful defibrillation, abstract..Clin Res 1983;3h208A. 17. Melker Rl, Cavallaro DL: Synchronous and asynchronous ventilation during cardiopulmonary resuscitation, abstract. Arm Emerg Med 1983;12:142.
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VENTILATION DURING CPR Melker
18. Sellick BA: Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet 1961;2:404406.
19. Salem MR, Wong AY, Mani M: Efficacy of cricoid pressure in preventing gastric inflation during bag-mask ventilation in pediatric patients. Anesthesiology 1974;40:96-98.
Preclinical Studies of Abdominal Counterpulsation in CPR Charles F Babbs, MD, PhD / West Lafayette, Indiana
Abdominal counterpulsation added to standard cardiopulmonary resuscitation improves blood flow in animal models when compared to chest compressions alone. Similar effects can be demonstrated in analog and digital computer models of the circulation. The technique generates both central aortic and central venous pressure pulses, and successful application of the method depends on maximizing the former and minimizing the latter. Proper technique is important in order to generate the largest possible arteriovenous pressure difference. [Babbs CF: Preclinical studies of abdominal counterpulsation in CPR. Ann Emerg Med September 1984 (Part 2);13:761-763. Key words: abdominal counterpulsation; cardiopulmonary resuscitation.]
Introduction The technique of abdominal counterpulsation during cardiopulmonary resuscitation (CPR) consists of applying external pressure to the abdomen during "diastole," the chest relaxation phase. During interposed abdominal compression-CPR (IAC-CPR), abdominal pressure is maintained manually over the midabdomen for 50% of cycle time, exactly 180 degrees out of phase with chest Compressions. A folded blood pressure cuff placed between the hands and the abdomen and connected to an aneroid manometer may be used to monitor the pressure applied. We have obtained good results with negligible trauma in animals using applied abdominal pressures of 120 to 150 m m Hg.
Hemodynamic Effects in the Canine Arrest Model The hemodynamic effects of abdominal counterpulsation have been discovered independently by several research teams in the last decade. In 1976 Ohomoto and coworkers 1 at Tokyo Women's Medical College described an arrangement of two mechanical pistons, one that compressed the chest and another that compressed the abdomen. They termed the technique "counter-massage," and found in preliminary studies that phased abdominal compression for 80% of cycle time and chest compression for 25% of cycle time appeared to improve carotid flow, mean aortic presFrom the Biomedical Engineering Center, Purdue University, West Lafayette, indiana. Address for reprints: Charles F Babbs, MD, PhD, Biomedical Engineering Center, AA Potter Building, Room 204, Purdue University, West Lafayette, indiana 47907. Supported by Research Career Development Award HL-00587 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. 12/761
sure, and short-term survival in anesthetized dogs with ventAcular fibrillation. Rosborough and coworkers 2 in Houston, while attempting to mimic the physiology of "cough-CPR" in an animal model, 3 combined simultaneous high-pressure lung inflation with abdominal compression. They found that abdominal compression and ventilation alone could maintain carotid flow and aortic blood pressure during ventricular fibrillation in dogs, and they suggested the technique as a new CPR modality. In 1981 Ralston, of Purdue University, observed the hemodynamic effects of interposed abdominal compressions as an adjunct to mechanical chest compression in dogs. 4 Interposed abdominal compressions dramatically improved brachial artery blood pressure without a comparable increase in central venous pressure {Figure 1). A subsequent controlled study of IAC-CPR in ten dogs with electrically induced fibrillation showed that the technique significantly improved cardiac output and diastolic arterial pressures. 4 In this study cardiac output was measured with an indicator dilution method specially modified for CPR, s and constant pressure {20 cm H20 ) ventilation was used. Voorhees et al6 at Purdue have continued this line of research and have shown an approximate doubling of cardiac output, diastolic arterial pressure, and diastolic arteriovenous pressure difference, with significant improvement in total body oxygen deliver~, when IAC was added to otherwise standard CPR {Figure 2). In this second study a specially modified spirometer recorded oxygen consumption during CPR. Cardiac output was measured by the Fick technique (0 2 consumption/A-V O 2 difference), and constant volume rather than constant pressure ventilation was applied. At about the same time Coletti and coworkers in New York were studying the influence of abdominal counterpulsation on cerebral and coronary blood flow in a canine model of cardiogenic shock.e,8 They found that when manual abdominal compressions were interposed between heartbeats (as judged from the ECG trace}, both carotid and coronary flow, measured with implanted electromagnetic probes, increased. The recent study by Walker and coworkers in Detroit 9 has confirmed the earlier animal experiments. These investigators measured perfusion of the cerebral cortex during IAC versus standard CPR in a canine model. They used both manual chest and manual abdominal compression in
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