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Open-chest CPR: An old method whose time has returned
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 2, Number 6
Open-chest CPR: An Old Method Whose Time Has Returned Although few seriously question the hemodynamic superiority of open-chest cardiopulmonary resuscitation (OCCPR) over standard external CPR (SECPR), the question remains: when does opening the chest offer an advantage over SECPR? We believe the indications for OCCPR ought to be clinically re-evaluated and widened to include cases of prolonged arrest time and failure of SECPR with drugs and countershock to promptly restart spontaneous circulation. EXPERIMENTAL STUDIES Open-chest CPR was first used by Schiff, in dogs, in the treatment of chloroform-induced cardiac arrest in 1874.’ Boehm2 reported in 1878 that external chest compressions could also return a rhythmic heart beat, but it was not until 1908 that Pike et al3 commented on the relative efficacy of the two techniques: “Often a faithful trial of extrathoracic massage has failed to start the heart. In nearly all of these cases direct massage has afterward proved effective.” During the next half century of widespread clinical use, there was little experimental evaluation of OCCPR. The reintroduction of SECPR into clinical practice by Kouwenhoven et al4 in 1960 stimulated experimental comparisons of the two techniques. The first such comparison was by Redding and Cozinej who showed similar common carotid artery blood flow (CCABF), arterial pressures and cardiac resuscitability with the two methods. Weale and Rothwell-Jackson6 found higher arterial and lower venous pressures during OCCPR than during SECPR in dogs, and also suggested that flow during external CPR is generated by overall intrathoracic pressure fluctuations (chest-pump mechanism). This was in contrast to direct heart compressions (heartpump mechanism) postulated by Kouwenhoven et af.4 The chest-pump mechanism of SECPR was recently documented by Weisfeldt et al.’ Weiser and coworkers found unequivocally better cardiac output during OCCPR than during SECPR. Yashon et al’ demonstrated the ability of OCCPR to restore and maintain essentially normal EEG activity for up to one hour after arrest times of less than 4 minutes. Gamelli and co-workers suggested possible cerebral metabolic benefits of OCCPR by demonstrating a nearly normal cerebral blood flow (CBF) equivalent (cerebral arteriovenous 0, content difference). Our studies demonstrated better CCABF and arteSupported by the NIH, the Asmund S. Laerdal Foundation, the Western Pennsylvania Heart Association, the Emergency Medicine Foundation, and the Pennsylvania Department of Health.
568
rial pressures and return of EEG activity in dogs by switching to OCCPR after prolonged SECPR.” Prolonged OCCPR gave better cardiac and cerebral resuscitability than either SECPR or “MAST”-augmented SECPR.“,” After two hours of SECPR and so-called “new” external CPR (simultaneous high pressure ventilation and compressions),’ OCCPR with the descending aorta cross-clamped provided better CCABF, cerebral arterio-venous perfusion pressure and cerebral venous Po,. I4 After 4 minutes of ventricular fibrillation without CPR, OCCPR for 30 minutes consistently led to prompt restoration of spontaneous circulation and gave a normal neurological status at 24 hours, which is a result no different from immediate defibrillation, while dogs receiving 30 minutes of SECPR or “new” CPR were usually brain dead.ls Finally, we found that external chest compressions caused high intrathoracic, venous, and intracranial pressure peaks, which resulted in very low cerebral perfusion pressures, whereas OCCPR produced low venous and intracranial pressures and high cerebral perfusion pressures. ‘l-l5 This suggests a shift of blood flow from brain to face during chest compressions, and from face to brain during OCCPR. Changes in CCABF reflect changes in CBF plus extracerebral flow. Therefore, direct measurements of CBF during CPR are needed. A CPR method should produce at least 20% of normal CBF to maintain brain tissue viability. l6 Byrne et al” were the first to measure CBF during OCCPR, using microspheres. They could maintain nearly normal CBF in dogs during OCCPR after 1 minute of arrest, whereas SECPR yielded only a third of the normal CBF. We measured CBF with the more reliable hydrogen clearance method and found SECPR to produce CBF values of nearly 20% after l-3 minutes of arrest in rabbits but after longer arrest times it produced only a trickle of flow, with zero CBF after 7 minutes of arrest.18 In contrast, we found OCCPR in dogs to produce nearly normal CBF after 1 minute of arrest and still-acceptable CBF after over 5 minutes of arrest.lY Barsan and Levy” obtained 17% of control cardiac output with SECPR, but up to 70% with OCCPR. Sanders and coworkers21 demonstrated markedly improved cardiac resuscitability using OCCPR. Clearly, the vast majority of experimental evidence favors the use of OCCPR over SECPR or any of its modifications, including interposed abdominal compression CPR, recently proposed by Voorhees et ~11.~~ The latter method produced, after short arrest times, only a minimal in-
OPEN-CHEST
crease of CBF over that during SECPR, 11.9% to 13.3% of normal.23
i.e. from
CLINICAL REPORTS The first reported attempt of OCCPR in humans was by Niehans, likely in 1899.24 Several more attempts were made prior to the first success by Igelsrud, probably in 1901.25 Although open-chest cardiac defibrillation had been worked out in animals at the turn of this century,26 it was not used until Beck and coworkers27 pioneered internal defibrillation in 1947. By 1953, Stephenson et UP* had accumulated 1,200 cases of cardiac arrest, of which 28% survived. In that series, 14% of the resuscitation attempts were initiated outside the operating room (inside the hospital), with a 17% survival rate. Adelson29 noted the incidence of complications resulting from OCCPR; gross laceration of the heart was present in 10% of cases, but massage could be performed successfully and without cardiac damage beyond one hour. The clinical techniques of OCCPR, practiced widely before 1960, have been discussed in other reports.27,28,30-36 The experiences reported were confirmed recently by interviews of the above authors3’-36 (Patrick McNulty, M.D., University of Pittsburgh, 1981, unpublished data), and included: physicians of various disciplines performing OCCPR, even in emergency departments; restoration of spontaneous circulation with drugs, fluids and countershocks facilitated by the visual control and “touch” provided by OCCPR; and most patients either recovering with good brain function (even after 1-2 hours of OCCPR), or dying. With the popularization of external cardiac massage by Kouwenhoven et al4 in 1960, OCCPR was relegated to the management of selected cases of cardiac arrest associated with intrathoracic trauma. Anecdotes continued to be reported, however. Russe1137reported survival after 2V2 hours of OCCPR. Sykes and Ahmed3’ reported comparable survivorship for internal and external CPR comparing two consecutive three-year periods; they concluded that OCCPR should be reserved for failure to respond to SECPR. Shocket and Rosenblum39 noted successful resuscitation with OCCPR in one patient after 75 minutes of external CPR had failed to restore a pulse; the patient eventually returned to his work as a stock-broker. MacKenzie et a140 recorded high right-atria1 pressures, low perfusion pressures, and low cardiac output in patients during SECPR and suggested that the role of OCCPR be re-evaluated. They also suggested that high central venous pressures might adversely influence cerebral outcome and that switching to OCCPR should be considered if artificial circulation was to be
CPR
needed for more than a few minutes. Del Guercio et aP4 reported significantly better cardiac indices with OCCPR in patients, as compared with SECPR. In the only study of the incidence of infection after emergency thoracotomy, Altemeier and Todd4r reported a surprisingly low rate of 2/43 patients. In neither case was the infection fatal, and, indeed, we know of no reported instances of patients dying as a result of wound infection from OCCPR for any indication. Stephenson29 provided a well-documented and reasoned review of indications for OCCPR in 1974. Despite this, the use of OCCPR was subsequently entirely relegated to cases of thoracic trauma. In such cases it is a standard42-46 although not entirely uncontroversial47 treatment. In these recent series, the incidences of wound infection ranged from 0.0% to 9.1%, and the incidences of iatrogenic heart damage ranged from 0.0% to 1.4%. Clearly, these are acceptable risks if substantial improvement in neurological outcome can be expected.44 There are now 5 nationahy and internationally recommended indications for 0CCPR:36 1) chest already open (in operating room); 2) suspected intrathoracic trauma; 3) suspected massive pulmonary embolism; 4) cardiac arrest with deep hypothermia; and 5) no artificial large artery pulse produced by SECPR. We would add a sixth indication: suspected long arrest time (as in unwitnessed arrest) followed by failure of correctly performed SECPR advanced life support efforts (with epinephrine, NaHCOX, and countershocks) to promptly (within 5 minutes) restore spontaneous circuIation. For external and interna CPR attempts, prompt restoration of adequate spontaneous circulation is more important than differences in blood flow produced during prolonged heart (chest) pumping. Ideally, OCCPR should be performed by a fully trained thoracic surgeon, but any physician can be trained to perform this procedure in a safe and expeditious fashion. In the absence of training, external CPR should be used. Dog laboratory practice sessions, used effectively before 1960 for OCCPR training,33q36 are no longer available to all medical students and physicians Therefore, a realistic OCCPR training manikin is needed. There is considerable evidence to suggest that OCCPR may be more efficacious than external CPR and that the risks of thoracotomy may be acceptable. Patients who respond to conventional advanced life support in the first 10 minutes of resuscitation are unlikely to have gained benefit from OCCPR. The clinical benefit of OCCPR to the nonresponders remains to be defined, but it may be immense. Internal and external CPR methods should be compared in a randomized, prospective clinical trial for cases of nontraumatic cardiac arrest to estabhsh the benefit of 569
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 2,
OCCPR for those patients who do not rapidly respond to external CPR. NICHOLASBIRCHER,MD PETERSAFAR, MD University of Pittsburgh and Presbyterian-University Hospital Pittsburgh, Pennsylvania
REFERENCES 1. Hake TG. Studies on ether and chloroform from Prof. Schiff’s physiological laboratory. Practitioner 1874; 12:241. 2. Boehm Ft. Ueber Wiederbelebung nach Vergiftungen und Asphyxie. Arch Exp Path Pharmocol 1878;8:88-101. 3. Pike FH, Guthrie CC, Stewart GN. Studies in resuscitation: I. The general conditions affecting resuscitation, and the resuscitation of the blood and of the heart. J Exp Med 1908;10:371-418. 4. Kouwenhoven WB, Jude JB, Knickerbocker GG. Closedchest cardiac massage. JAMA 1980;173:1064-1067. of open-chest and 5. Redding JS, Cozine R. A comparison closed-chest cardiac massage in dogs. Anesthesiology 1961;22:280-285. 6. Weale FE, Rothwell-Jackson RL. The efficiency of cardiac massage. Lancet 1962;1:990-992. 7. Weisfeldt ML, Chandra N, Tsitlik J. Increased intrathoracic pressure-not direct heart compression-causes the rise in intrathoracic vascular pressures during CPR in dogs and pigs. Crit Care Med 1981;9:377-378. 8. Weiser FM, Adler LN, Kuhn LA. Hemodynamic effects of closed and open-chest cardiac resuscitation in normal dogs and those with acute myocardial infarction. Am J Cardiol 1962;10:555-561. 9. Yashon D, Wagner FC, Massopust LC, et al. Electrocorticographic limits of cerebral viability during cardiac arrest and resuscitation. Am J Surg 1971;121:728-731. 10. Gamelli R, Saucier J, Browdie D. An analysis of cerebral blood flow systemic base deficit and mean arterial pressure as a function of internal cardiac massage rates. Am Surg 1979;45:26-33. 11. Bircher N, Safar P, Stewart R. A comparison of standard, “MAST’‘-augmented and open-chest CPR in dogs: A preliminary investigation. Crit Care Med 1980;8:147-152. 12. Alifimoff JK, Safar P, Bircher N, et al. Cardiac resuscitability after closed-chest, MAST-augmented and open-chest cardiopulmonary resuscitation (CPR). Anesthesiology 1980;53(Suppl):S151. 13. Alifimoff JK, Safar P, Bircher N, et al. Cerebral recovery after prolonged closed-chest, MAST-augmented and openchest cardiopulmonary resuscitation (CPR). Anesthesiology 1980;53(Suppl):S147. 14. Bircher N, Safar P. Comparison of standard and “new” closed-chest CPR and open-chest CPR in dogs. Crit Care Med 1981;9:384-385. 15. Bircher NG, Safar P. Cerebral preservation during cardiopulmonary resuscitation (CPR) in dogs. Anesthesiology 1983;59(Suppl):A93. 16. Astrup J, Symon L, Branston NM, et al. Cortical evoked potential in extracellular K+ and H+ at critical levels of brain ischemia. Stroke 1977;8:51-57. 17. Byrne D, Pass HI, Neely WA, et al. External versus internal cardiac massage in normal and chronically ischemic dogs. Am Surg 1980;46:657-662. 18. Lee SK, Vaagenes P, Safar P, et al. Effect of cardiac arrest time on cortical cerebral blood flow generated by sub570
nber 6
19.
20.
21.
22.
23.
24. 25.
26.
27.
28.
29.
30.
31. 32. 33.
34.
35.
36.
37.
38. 39.
sequent standard external cardiopulmonary resuscitation in rabbits. Ann Emerg Med 1984 (in press). Stadjuhar K, Steinberg, R, Sotosky M, et al. Cerebral blood flow (CBF) and common carotid artery blood flow (CCABF) during open-chest cardiopulmonary resuscitation (OCCPR) in dogs. Anesthesiology 1983;59 (Suppl):All7. Barsan WG, Levy RC. Experimental design for study of cardiopulmonary resuscitation in dogs. Ann Emerg Med 1981;10:135-137. Sanders AB, Kern K, Ewy GA, et al. Improved survival from cardiac arrest with open-chest massage. Ann Emerg Med 1983;12:138. Voorhees WD, Niebauer MJ, Babbs CF. Improved oxygen delivery during cardiopulmonary resuscitation with interposed abdominal compressions. Ann Emerg Med 1983;12:128-135. Voorhees WD, Niebauer MJ, Babbs CF. Regional blood flow during CPR with abdominal counter-pulsation in dogs. Am J Emerg Med 1984;2:123-128. Zesas DG. Uber Massage des freigelegten Herzens beim Chloroformkollaps. Zentralbl Chir 1903;23:588-590. Keen WW. A case of total laryngectomy (unsuccessful) and a case of abdominal hysterectomy (successful), in both of which massage of the heart for chloroform collapse was employed, with notes of 25 other cases of cardiac massage. Ther Gaz 1904;28:217-230. Prevost JL, Battelli F. On some effects of electrical discharges on the hearts of mammals. CR Seances Acad Sci (Ill) 1899;129:1267. Beck CS, Pritchard WH, Feil HS. Ventricular fibrillation of long duration abolished by electric shock. JAMA 1947;135:985-986. Stephenson HE, Reid C, Hinton JW. Some common denomination in 1200 cases of cardiac arrest. Ann Surg 1953;137:731-744. Adelson L: A clinicopathologic study of the anatomic changes in the heart resulting from cardiac massage. Surg Gyn Obst 1957;104:513-523. Stephenson HE. Closed-chest massage versus direct heart manual compression of the heart. In Stephenson HE (ed). Cardiac Arrest and Resuscitation. St. Louis: C. V. Mosby, 1974:324-335. Dripps RD, Kirby CK, Johnson J, et al. Cardiac resuscitation Ann Surg 1948;127:592-604. Johnson J, Kirby CK. Surgery of the Chest. Chicago: Yearbook Medical Publishers, 1964. Leighninger DS. Contributions of Claude Beck. In Safar P (ed). Advances in Cardiopulmonary Resuscitation. New York: Springer-Verlag, 1977:259-262. Del Guercio LRM, Feins NR, Cohn JD, et al. Comparison of blood flow during external and internal cardiac massage in man. Circulation 1964;29/3O(Suppl lll):lll-67; and 1965;31/32(Suppl l):l-171-I-180. Ravitch M, Lane R, Safar P, et al. Lightning stroke: Recovery following cardiac massage and prolonged artificial respiration. New Engl J Med 1961;264:36-38. Safar P. Cardiopulmonary Cerebral Resuscitation: A Manual for Physicians and Paramedical Instructors (World Federations of Societies of Anaesthesiologists). Philadelphia: W. B. Saunders, 1981:172-174. Russell ES. Cardiac arrest: A. Survival after 2% hours openchest cardiac massage, and B. Survival after closed-chest cardiac massage. Can Med Assoc J 1962;87:512-513. Sykes MK, Ahmed N. Emergency treatment of cardiac arrest. Lancet 1963;2:347-349. Shocket E, Rosenblum R. Successful open cardiac massage
OPEN-CHEST
40.
41.
42. 43.
after 75 minutes of closed massage. JAMA 1967;200:333335. MacKenzie GJ, Taylor SH, McDonald AH, et al. Haemodynamic effects of external cardiac compression. Lancet 1964;1:1342-1345. Altermeier WA, Todd J. Studies on the incidence of infection following open-chest cardiac massage for cardiac arrest. Ann Surg 1963;158:596-604. Mattox KL, Espada R, Beall AC, et al. Performing thoracotomy in the emergency center. JACEP 1974;3:13-17. Mattox KL, Beall AC, Jordan GL, et al. Cardiorrhaphy in the emergency center. J Thorac Cardiovasc Surg 1974; 68:886-895.
CPR
44. Baker CC, Caronna JJ, Trunkey DD. Neurologic outcome after emergency room thoracotomy for trauma. Am J Surg 1980;139:677-681. 45. Baker CC, Thomas AN, Trunkey DD. The role of emergency room thoracotomy in trauma. J Trauma 1980;20:848-855. 46. lvatury RR, Shah PM, Ito K, et al. Emergency room thoracotomy for the resuscitation of patients with “fatal” penetrating injuries of the heart. Ann Thorac Surg 1981;32:377-385. 47. Moore EE, Moore JB, Galloway AC, et al. Post-injury thoracotomy in the emergency room: A critical evaluation. Surgery 1979;86:590-598.
571
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 2, Number 6
Open-chest CPR: An Old Method Whose Time Has Returned Although few seriously question the hemodynamic superiority of open-chest cardiopulmonary resuscitation (OCCPR) over standard external CPR (SECPR), the question remains: when does opening the chest offer an advantage over SECPR? We believe the indications for OCCPR ought to be clinically re-evaluated and widened to include cases of prolonged arrest time and failure of SECPR with drugs and countershock to promptly restart spontaneous circulation. EXPERIMENTAL STUDIES Open-chest CPR was first used by Schiff, in dogs, in the treatment of chloroform-induced cardiac arrest in 1874.’ Boehm2 reported in 1878 that external chest compressions could also return a rhythmic heart beat, but it was not until 1908 that Pike et al3 commented on the relative efficacy of the two techniques: “Often a faithful trial of extrathoracic massage has failed to start the heart. In nearly all of these cases direct massage has afterward proved effective.” During the next half century of widespread clinical use, there was little experimental evaluation of OCCPR. The reintroduction of SECPR into clinical practice by Kouwenhoven et al4 in 1960 stimulated experimental comparisons of the two techniques. The first such comparison was by Redding and Cozinej who showed similar common carotid artery blood flow (CCABF), arterial pressures and cardiac resuscitability with the two methods. Weale and Rothwell-Jackson6 found higher arterial and lower venous pressures during OCCPR than during SECPR in dogs, and also suggested that flow during external CPR is generated by overall intrathoracic pressure fluctuations (chest-pump mechanism). This was in contrast to direct heart compressions (heartpump mechanism) postulated by Kouwenhoven et af.4 The chest-pump mechanism of SECPR was recently documented by Weisfeldt et al.’ Weiser and coworkers found unequivocally better cardiac output during OCCPR than during SECPR. Yashon et al’ demonstrated the ability of OCCPR to restore and maintain essentially normal EEG activity for up to one hour after arrest times of less than 4 minutes. Gamelli and co-workers suggested possible cerebral metabolic benefits of OCCPR by demonstrating a nearly normal cerebral blood flow (CBF) equivalent (cerebral arteriovenous 0, content difference). Our studies demonstrated better CCABF and arteSupported by the NIH, the Asmund S. Laerdal Foundation, the Western Pennsylvania Heart Association, the Emergency Medicine Foundation, and the Pennsylvania Department of Health.
568
rial pressures and return of EEG activity in dogs by switching to OCCPR after prolonged SECPR.” Prolonged OCCPR gave better cardiac and cerebral resuscitability than either SECPR or “MAST”-augmented SECPR.“,” After two hours of SECPR and so-called “new” external CPR (simultaneous high pressure ventilation and compressions),’ OCCPR with the descending aorta cross-clamped provided better CCABF, cerebral arterio-venous perfusion pressure and cerebral venous Po,. I4 After 4 minutes of ventricular fibrillation without CPR, OCCPR for 30 minutes consistently led to prompt restoration of spontaneous circulation and gave a normal neurological status at 24 hours, which is a result no different from immediate defibrillation, while dogs receiving 30 minutes of SECPR or “new” CPR were usually brain dead.ls Finally, we found that external chest compressions caused high intrathoracic, venous, and intracranial pressure peaks, which resulted in very low cerebral perfusion pressures, whereas OCCPR produced low venous and intracranial pressures and high cerebral perfusion pressures. ‘l-l5 This suggests a shift of blood flow from brain to face during chest compressions, and from face to brain during OCCPR. Changes in CCABF reflect changes in CBF plus extracerebral flow. Therefore, direct measurements of CBF during CPR are needed. A CPR method should produce at least 20% of normal CBF to maintain brain tissue viability. l6 Byrne et al” were the first to measure CBF during OCCPR, using microspheres. They could maintain nearly normal CBF in dogs during OCCPR after 1 minute of arrest, whereas SECPR yielded only a third of the normal CBF. We measured CBF with the more reliable hydrogen clearance method and found SECPR to produce CBF values of nearly 20% after l-3 minutes of arrest in rabbits but after longer arrest times it produced only a trickle of flow, with zero CBF after 7 minutes of arrest.18 In contrast, we found OCCPR in dogs to produce nearly normal CBF after 1 minute of arrest and still-acceptable CBF after over 5 minutes of arrest.lY Barsan and Levy” obtained 17% of control cardiac output with SECPR, but up to 70% with OCCPR. Sanders and coworkers21 demonstrated markedly improved cardiac resuscitability using OCCPR. Clearly, the vast majority of experimental evidence favors the use of OCCPR over SECPR or any of its modifications, including interposed abdominal compression CPR, recently proposed by Voorhees et ~11.~~ The latter method produced, after short arrest times, only a minimal in-
OPEN-CHEST
crease of CBF over that during SECPR, 11.9% to 13.3% of normal.23
i.e. from
CLINICAL REPORTS The first reported attempt of OCCPR in humans was by Niehans, likely in 1899.24 Several more attempts were made prior to the first success by Igelsrud, probably in 1901.25 Although open-chest cardiac defibrillation had been worked out in animals at the turn of this century,26 it was not used until Beck and coworkers27 pioneered internal defibrillation in 1947. By 1953, Stephenson et UP* had accumulated 1,200 cases of cardiac arrest, of which 28% survived. In that series, 14% of the resuscitation attempts were initiated outside the operating room (inside the hospital), with a 17% survival rate. Adelson29 noted the incidence of complications resulting from OCCPR; gross laceration of the heart was present in 10% of cases, but massage could be performed successfully and without cardiac damage beyond one hour. The clinical techniques of OCCPR, practiced widely before 1960, have been discussed in other reports.27,28,30-36 The experiences reported were confirmed recently by interviews of the above authors3’-36 (Patrick McNulty, M.D., University of Pittsburgh, 1981, unpublished data), and included: physicians of various disciplines performing OCCPR, even in emergency departments; restoration of spontaneous circulation with drugs, fluids and countershocks facilitated by the visual control and “touch” provided by OCCPR; and most patients either recovering with good brain function (even after 1-2 hours of OCCPR), or dying. With the popularization of external cardiac massage by Kouwenhoven et al4 in 1960, OCCPR was relegated to the management of selected cases of cardiac arrest associated with intrathoracic trauma. Anecdotes continued to be reported, however. Russe1137reported survival after 2V2 hours of OCCPR. Sykes and Ahmed3’ reported comparable survivorship for internal and external CPR comparing two consecutive three-year periods; they concluded that OCCPR should be reserved for failure to respond to SECPR. Shocket and Rosenblum39 noted successful resuscitation with OCCPR in one patient after 75 minutes of external CPR had failed to restore a pulse; the patient eventually returned to his work as a stock-broker. MacKenzie et a140 recorded high right-atria1 pressures, low perfusion pressures, and low cardiac output in patients during SECPR and suggested that the role of OCCPR be re-evaluated. They also suggested that high central venous pressures might adversely influence cerebral outcome and that switching to OCCPR should be considered if artificial circulation was to be
CPR
needed for more than a few minutes. Del Guercio et aP4 reported significantly better cardiac indices with OCCPR in patients, as compared with SECPR. In the only study of the incidence of infection after emergency thoracotomy, Altemeier and Todd4r reported a surprisingly low rate of 2/43 patients. In neither case was the infection fatal, and, indeed, we know of no reported instances of patients dying as a result of wound infection from OCCPR for any indication. Stephenson29 provided a well-documented and reasoned review of indications for OCCPR in 1974. Despite this, the use of OCCPR was subsequently entirely relegated to cases of thoracic trauma. In such cases it is a standard42-46 although not entirely uncontroversial47 treatment. In these recent series, the incidences of wound infection ranged from 0.0% to 9.1%, and the incidences of iatrogenic heart damage ranged from 0.0% to 1.4%. Clearly, these are acceptable risks if substantial improvement in neurological outcome can be expected.44 There are now 5 nationahy and internationally recommended indications for 0CCPR:36 1) chest already open (in operating room); 2) suspected intrathoracic trauma; 3) suspected massive pulmonary embolism; 4) cardiac arrest with deep hypothermia; and 5) no artificial large artery pulse produced by SECPR. We would add a sixth indication: suspected long arrest time (as in unwitnessed arrest) followed by failure of correctly performed SECPR advanced life support efforts (with epinephrine, NaHCOX, and countershocks) to promptly (within 5 minutes) restore spontaneous circuIation. For external and interna CPR attempts, prompt restoration of adequate spontaneous circulation is more important than differences in blood flow produced during prolonged heart (chest) pumping. Ideally, OCCPR should be performed by a fully trained thoracic surgeon, but any physician can be trained to perform this procedure in a safe and expeditious fashion. In the absence of training, external CPR should be used. Dog laboratory practice sessions, used effectively before 1960 for OCCPR training,33q36 are no longer available to all medical students and physicians Therefore, a realistic OCCPR training manikin is needed. There is considerable evidence to suggest that OCCPR may be more efficacious than external CPR and that the risks of thoracotomy may be acceptable. Patients who respond to conventional advanced life support in the first 10 minutes of resuscitation are unlikely to have gained benefit from OCCPR. The clinical benefit of OCCPR to the nonresponders remains to be defined, but it may be immense. Internal and external CPR methods should be compared in a randomized, prospective clinical trial for cases of nontraumatic cardiac arrest to estabhsh the benefit of 569
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 2,
OCCPR for those patients who do not rapidly respond to external CPR. NICHOLASBIRCHER,MD PETERSAFAR, MD University of Pittsburgh and Presbyterian-University Hospital Pittsburgh, Pennsylvania
REFERENCES 1. Hake TG. Studies on ether and chloroform from Prof. Schiff’s physiological laboratory. Practitioner 1874; 12:241. 2. Boehm Ft. Ueber Wiederbelebung nach Vergiftungen und Asphyxie. Arch Exp Path Pharmocol 1878;8:88-101. 3. Pike FH, Guthrie CC, Stewart GN. Studies in resuscitation: I. The general conditions affecting resuscitation, and the resuscitation of the blood and of the heart. J Exp Med 1908;10:371-418. 4. Kouwenhoven WB, Jude JB, Knickerbocker GG. Closedchest cardiac massage. JAMA 1980;173:1064-1067. of open-chest and 5. Redding JS, Cozine R. A comparison closed-chest cardiac massage in dogs. Anesthesiology 1961;22:280-285. 6. Weale FE, Rothwell-Jackson RL. The efficiency of cardiac massage. Lancet 1962;1:990-992. 7. Weisfeldt ML, Chandra N, Tsitlik J. Increased intrathoracic pressure-not direct heart compression-causes the rise in intrathoracic vascular pressures during CPR in dogs and pigs. Crit Care Med 1981;9:377-378. 8. Weiser FM, Adler LN, Kuhn LA. Hemodynamic effects of closed and open-chest cardiac resuscitation in normal dogs and those with acute myocardial infarction. Am J Cardiol 1962;10:555-561. 9. Yashon D, Wagner FC, Massopust LC, et al. Electrocorticographic limits of cerebral viability during cardiac arrest and resuscitation. Am J Surg 1971;121:728-731. 10. Gamelli R, Saucier J, Browdie D. An analysis of cerebral blood flow systemic base deficit and mean arterial pressure as a function of internal cardiac massage rates. Am Surg 1979;45:26-33. 11. Bircher N, Safar P, Stewart R. A comparison of standard, “MAST’‘-augmented and open-chest CPR in dogs: A preliminary investigation. Crit Care Med 1980;8:147-152. 12. Alifimoff JK, Safar P, Bircher N, et al. Cardiac resuscitability after closed-chest, MAST-augmented and open-chest cardiopulmonary resuscitation (CPR). Anesthesiology 1980;53(Suppl):S151. 13. Alifimoff JK, Safar P, Bircher N, et al. Cerebral recovery after prolonged closed-chest, MAST-augmented and openchest cardiopulmonary resuscitation (CPR). Anesthesiology 1980;53(Suppl):S147. 14. Bircher N, Safar P. Comparison of standard and “new” closed-chest CPR and open-chest CPR in dogs. Crit Care Med 1981;9:384-385. 15. Bircher NG, Safar P. Cerebral preservation during cardiopulmonary resuscitation (CPR) in dogs. Anesthesiology 1983;59(Suppl):A93. 16. Astrup J, Symon L, Branston NM, et al. Cortical evoked potential in extracellular K+ and H+ at critical levels of brain ischemia. Stroke 1977;8:51-57. 17. Byrne D, Pass HI, Neely WA, et al. External versus internal cardiac massage in normal and chronically ischemic dogs. Am Surg 1980;46:657-662. 18. Lee SK, Vaagenes P, Safar P, et al. Effect of cardiac arrest time on cortical cerebral blood flow generated by sub570
nber 6
19.
20.
21.
22.
23.
24. 25.
26.
27.
28.
29.
30.
31. 32. 33.
34.
35.
36.
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