- Email: [email protected]
Pressures during manual and mechanical CPR
At that time emergency medicine had access neither to the Liaison Committee for Graduate Medical Education nor to the c o m m i t t e e staff. Emergency medicine could not afford to engage full-time site surveyors, and thus by necessity developed a core of surveyors from among the faculties of various residency programs in emergency medicine. To avoid individual bias and to put forth the best possible effort, two surveyors were assigned to each visit. The fact that surveyors, by and large, were highly motivated, knowledgeable emergency physicians did not preclude many problems, concerns, and complaints related to their surveys. As a result, a relatively large number of individuals performed only two or three surveys each, which limited their in-depth knowledge and familiarity with the institution and other graduate medical education programs in that locale. It was with full and complete knowledge of the forthcoming changes that the leadership of emergency medicine willingly exchanged the intramural LREC for the extramural, nationwide and professionwide RRC/ACGME, with the result that basic and initial reviews are done by the Council's field staff. The ,initial experience of the RRC-EM with the quality, depth, and perceptiveness of surveys by the field staff has been positive and satisfactory. Staff reports were reviewed in depth by the RRC as well as by a panel of the Council. The RRC-EM has reserved the right (and, in fact, has already used the right) to dispatch specialist site visitors (emergency physicians) where it has been necessary. I would hope that Dr Skiendzielewski might be more patient, and would allow the RRC-EM to complete one full cycle of review and site visitation and allow the RRC to evaluate not only graduate medical education in emergency medicine, but also the process of review. From that point on, criticism, inquiry, and analysis will be in order. Change is always hard to accept, easy to resist, and likely to be perceived as a threat. It was inevitable that at some point the LREC activity would cease and the RRC would take over. Dr Skiendzielewski's program was the recipient of one of the earliest RRC visits. It may have been close on the heels of the LREC survey, but it had to occur at some time. The Residency Review Committee on Emergency Medicine is made up of ten dedicated emergency physicians who
were carefully selected to represent every conceivable configuration in emergency medicine. This committee is making every effort to maintain excellence in its review methodology, while maintaining awareness of available finances, resources, demands, and realities. Dr Skiendzielewski, and anyone else, should not hesitate to call to m y attention any problems, comments, and complaints dealing with the review mechanism as long as they are objective, useful, and documented. A comparison of backgrounds of the reviewers, the time spent at the institution, and the encounters with staff should not serve as the sole basis for complaints. Dr Skiendzielewski's initial contact with the residency review committee, although very brief, turned out to be positive for him. His judgment, however, in m y opinion, was arrived at in haste, was not entirely fair, and was expressed in a hyperbole that I, for one, do not expect from a director of a residency program in emergency medicine.
George Podgorny, MD, Chairman RRC-EM
To the Editor: Dr Skiendzielewski's point is well taken. Those of us who were active in the Liaison Residency Endorsement Committee recognized many imperfections in our endorsement process, but an indubitable strength was survey by physician peers - - a parallel to jury-by-peers. The closer and more familiar a surveyor to the scene at hand, the greater likelihood of a sophisticated and penetrating survey. The use of non-physician and non-specialty surveyors has been roundly criticized in other specialty organizations - - most particularly Surgery. Although there may be good reasons for the current use of non-physician, non-emergency-medicine surveyors, I agree with Dr Skiendzielewski that this practice should be carefully reviewed by the Residency Review Committee on Emergency Medicine. Robert H. Dailey, MD Past-Chairman Liaison Residency Endorsement Committee
Pressures During Manual and Mechanical CPR To the Editor: The article by McDonald, entitled "Systolic and Mean Arterial Pressures During Manual and Mechanical CPR in H u m a n s " {11:292-295, June 1982) is interesting, but presents several problems. First, the data presented do not justify the conclusion that, "Chest compression by a pneumatic device is superior . . . in producing higher mean arterial pressures (MAP)." A straightforward two-tailed test for a significant difference between the MAP data groups obtained with manual versus mechanical CPR reveals the following: 12:4 April 1983
Manual Mean = 24.9 m M Hg SD = 1 3 . 8 m M H g
Mechanical Mean = 31.9 m M Hg SD = 1 3 . 7 m M H g
with 28 degrees of freedom, t = 1.34. The probability that the two groups are not different is considerably greater than 10% (P > .1). Thus the null hypothesis that the two data groups represent random sampling from the same data pool is not excluded, and the difference is not statistically significant.
Annals of Emergency Medicine
267/115
CORRESPONDENCE
Second, the fact that there was zero survival in the series is troublesome. These outcome data can hardly be used to recommend either prolonged mechanical or m a n u a l CPR. Indeed, the fatal flaw m a y lie in prolonged closed chest CPR rather than in either the T h u m p e r ® or the hand. The ratio of live discharges to the n u m b e r of CPRs initiated outside the hospital varies from 5% to 20%. 1-s This n u m b e r includes patients w i t h p e r m a n e n t neurologic injury, and therefore the neurologically intact discharge rate is still lower. Bergner et al t have reported progressively poor outcome when definitive resuscitation (defibrillation) occurred more than six m i n u t e s following collapse, even w i t h immediate CPR initiation. Three series of patients w i t h prolonged CPR following rapid initiation of ALS were reported at the UAEM m e e t i n g last year. 6a Total patients in the pooled data from these series are 392. Of these, 88 were successfully resuscitated. Only 14 patients were discharged neurologically intact. Similar trends indicating very little cardiac or cerebral protection by early but prolonged CPR are also evident in the reports from Eisenberg. 4 Evidence is accumulating that the physiology involved in closed chest CPR m a y be responsible for the poor outcome data we are now forced to confront. The systolic arterial pulse produced by CPR is a result of elevated intrathoracic pressure, not ventricular compression. 9-1° Thus there is little t h o r a c i c a r t e r i o v e n o u s p e r f u s i o n p r e s s u r e gradient. N i e m a n n et al tl have recently reported the poor net coronary perfusion pressures. We have done cerebral cortical perfusion studies in dogs during CPR (mean systolic pressure = 75 m M Hg) demonstrating less than 10% of prearrest flow (.732 -+ .3 c c / m i n / g m vs .054. -+ .01 cc/min/gm) in the cerebal cortex with i m m e d i a t e initiation of CPR. t2 Kohler et a113 have reported similar data. Bircher and Safar 14 also have reported these low flows and demonstrated little improvement w i t h the so-called " n e w " CPR or abdominal binding. In contrast, cerebral cortical blood flow during internal cardiac massage is equal to or greater than prearrest perfusion, is This reflects substantially better cardiac output, as previously reported in patients, ~6 and also the production of arterial pressure by ventricular ejection without simultaneous massive elevation of thoracic venous pressures. Finally, the argument that the poor perfusion pressure and low flows generated by CPR are better than nothing can no longer be accepted uncritically. H o s s m a n n and Kleihues ~z and Nordstrom et al TM have studied brain no flow versus 10% flow. The data demonstrate a tenfold greater neuronal lactate accumulation and m u c h poorer ATP recovery with 10% flow. Mitochondrial injury is also exacerbated in the low flow m o d e ) 9 Thus the McDonald paper demonstrates low MAPs during CPR without any significant difference between m a n u a l and mechanical CPR. It does not report simultaneous CVPs, and thus net perfusion pressures cannot be discussed. It does provide another small series confirming the statistical futility of prolonged CPR. In this respect it serves to raise the issues reviewed here. In view of these issues revolving around CPR itself, further studies of " T h u m p e r ® vs pumper" would appear to have low priority at this time. 116/268
Blaine C. White, MD Department of Emergency Medicine Michigan State University East Lansing Carl D. Winegar, MD Paul J. Hoehner Raymond Jackson, MD Department of Emergency Medicine Detroit Receiving Hospital Detroit Kathleen Joyce, MD Department of Anesthesia Sinai Hospital Detroit 1. Bergner L, Eisenberg M, Hallstrom A, et al: Evaluation of paramedic services for cardiac arrest. US Department of Health and Human Services, National Center for Health Services Research Report (HS 02456), December 1981. 2. Eliastam M, Duralde T, Martinez F, et al: Cardiac arrest in the EMS system: Guidelines for resuscitation. JACEP 6:525-529, 1977. 3. Myerberg RJ, Kessler KM, Zaman L, et al: Survivors of prehospital cardiac arrest. JAMA 247:1485-1490, 1981. 4. Eisenberg MS, Copass MK, Hallstrom A: Management of out-ofhospital cardiac arrest - - Failure of basic EMT services. JAMA 243:1049-1051, 1980. 5. Nagel EL, Liberthson RR, Hirschman JC, et al: Emergency care. Circulation 52(Suppl 3):216, 1975. 6. Mahoney BD, Mirick MJ: Efficacy of pneumatic trousers in refractory prehospital cardiopulmonary arrest. Ann Emerg Med 12:812, 1983. 7. Campell DB, Hurvitz S, Hammon B, et al: Field vs emergency department resuscitation of out-of-hospital cardiac arrest. Presented at the UAEM Scientific Meeting, Salt Lake City, Utah, April 15-17, 1982. 8. Mirick MJ, Mahoney BD, Sherman R, et al: Refractory prehospital cardiac arrest: A contrast from previously reported prognostic indicators. Presented at the UAEM Scientific Meeting, Salt Lake City, Utah, April 15-17, 1982. 9. Rudikoff MT, Maughan WL, Effron M, et al: Mechanisms of blood flow during CPR. Circulation 61:345-352, 1980. 10. Niemarm JT, Rosborough JP, Haus Knecht M, et al: Pressure synchronized cineangiographic observations during experimental CPR. Circulation 64:985-991, 1981. 11. Niemann JT, Rosborough JP, Ung S, et al: Coronary perfusion pressure during experimental CPR. Ann Emerg Med 11:127-131, 1982. 12. Jackson R, Danosi S, White BC: Cerebral cortical perfusion during CPR and post-resuscitation: Presented at the International Scientific Symposium on Cerebral Resuscitation, Detroit, Michigan, July 7-8, 1982. 13. Kohler RC, Chandra N, Guerci AD, et al: Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding following cardiac arrest in dogs. Circulation (in press). 14. Bircher N, Safar P: Comparison of standard and "new" dosed chest CPR and open-chest CPR in dogs. Crit Care Med 9:384, 1981. 15. Joyce K, Vigor D, White BC: Perfusion of the cerebral cortex by
Annals of Emergency Medicine
12:4 April 1983
internal cardiac massage alter a 15-minute cardiac arrest in dogs. Presented at the International Scientific Symposium on Cerebral Resuscitation, Detroit, Michigan, July 7-8, 1982. 16. Del Guercio LRM, Feins NR, Cohn JD, et al: Comparison of blood flow during external and internal cardiac massage in man. Circulation 31-32(Suppl 1):I-171-I-180, 1965. 17. Hossman KA, Kleihues P: Reversibility of ischemic brain damage. Arch Neurol 29:375-382, 1973. 18. Nordstrom CH, Rehncrona S, Siesjo BK: Restitution of cerebral energy state after 30 minutes of complete ischemia in rats anesthetized with nitrous oxide or phenobarbital. J Neuroclhem 30:479-486, 1978. 19. Rehncrona S, Mela L, Siesjo BK: Recovery of brain mitochondrial function in the rat after complete and incomplete cerebral ischemia. Stroke 10:437-446, 1979.
To the Editor: We believe White et al have erred in their choice of a statistical method to help t h e m in their interpretation of our data. They have done an analysis using the two-tailed test for equality of two means. The use of this method, in this situation, is incorrect because the two sets of data w h i c h make up the samples are not independent. This is so because both sets of readings, manual vs mechanical, were t a k e n from the same set of patients. Furthermore they have Incorporated into their statistical treatment the large differences in pressures generated from patient to patient. Our study design eliminated the need to consider these differences, which are not pertinent. W h a t we did was to analyze data derived from the comparison of pressures obtained from matched pairs. 1 These m a t c h e d pairs are pressures generated in the same person by 1) mechanical and 2) manual chest compression. This is t e r m e d a "randomized block design." The appropriate test is the paired difference test. W i t h 14 degrees of freedom we obtained a t of - 2.84. The difference is statistically significant (P < .01), which justifies our excluding the null hypothesis. W h i t e et al further state that zero survival is troublesome. Our paper stated that all 15 persons were in the late stages of the resuscitative effort and, furthermore, that the data presented did not represent our typical experience in generating m e a n arterial pressures (MAPs) in persons who are in the early stages of the resuscitative process. Such persons were, by design, eliminated from our study because so m a n y other t r e a t m e n t modalities are typically utilized early in resuscitative efforts which could affect the pressures during the study and thus render the comparison invalid. To say that we r e c o m m e n d either prolonged mechanical or manual CPR is not correct. In our paper we clearly state that on m a n y occasions systolic arterial pressures which might be interpreted as consistent with continued brain survival were associated w i t h MAPs so low as to preclude the possibility of survival. This was true not only for some patients undergoing m a n u a l chest compression, but in some of those undergoing mechanical chest compression as well. 12:4 April 1983
What we intended to i m p l y was that in such instances, unless maneuvers could be accomplished to increase MAP w i t h i n a very short period of time, the resuscitative efforts should be discontinued. We are aware of the study of N i e m a n n et al ~ which indicates the poor net coronary perfusion pressure during closed chest CPR. We were not aware of this fact at the time the study was being performed. We are n o w s i m u l t a n e o u s l y measuring central venous and central arterial pressures during some of our resuscitative efforts. We have no disagreement w i t h the elaboration of the extremely poor results attendant to prolonged CPR. However, even with prolonged CPR, survival is greater than zero. And any technique which increases the rate of survival by even a small factor is worthwhile. We believe that our study indicates that u t i l i z a t i o n of m e c h a n i c a l chest compression, together w i t h rapid i m p l e m e n t a t i o n of MAP monitoring, can lead to a more sophisticated resuscitative effort. This could, in turn, lead to an increased rate of survival. Most studies emanate from large hospitals and teaching institutions which have available to t h e m at the time of resuscitation large n u m b e r s of h i g h l y skilled personnel. However, the vast preponderance of cardiac arrests occur in the prehospital care setting, in small emergency departments, and in critical care units in which only one or two people are available to perform the resuscitation. The use of a m e c h a n i c a l device to both compress the chest and to ventilate frees up the hands to perform other critically important tasks and, perhaps more important, flees up the m i n d to do decision m a k i n g w h i c h is of higher quality. The other points raised in the reply to our paper, we believe, are not so m u c h questions regarding our study but more a discourse on the current pattern of research being done by White's group and by others. We look forward enthusiastically to the results of these studies, and stand ready to change our methods when it is scientifically sound to do SO.
In summary, we believe our study does demonstrate that mechanical chest compression results in higher MAPs and could result in increased survival. Furthermore, we continue to urge those persons who are performing resuscitations and who have access to m o n i t o r i n g equipment to rapidly i m p l e m e n t MAP m e a s u r e m e n t early on in their resuscitative efforts. In closing, we agree w i t h White et al that further studies of " ' T h u m p e r ® vs pumper' appear to have a low priority" at this time. Instead, we should all be performing studies which will elucidate better methods of performing resuscitations so that we can increase the current miserably low rate of survival. John L. McDonald, M D Santa Rosa, California 1. Mendenhall W: Introduction to Probability and Statistics, ed 3. Belmont, CA, Duxbury Press, 1971, p 1035-1039. 2. Niemarm AP, Rosborough JP, Ung S, et al: Coronary perfusion pressure during experimental CPR. Ann Emerg Med 11:127-131, 1982.
Annals of Emergency Medicine
269/117
were carefully selected to represent every conceivable configuration in emergency medicine. This committee is making every effort to maintain excellence in its review methodology, while maintaining awareness of available finances, resources, demands, and realities. Dr Skiendzielewski, and anyone else, should not hesitate to call to m y attention any problems, comments, and complaints dealing with the review mechanism as long as they are objective, useful, and documented. A comparison of backgrounds of the reviewers, the time spent at the institution, and the encounters with staff should not serve as the sole basis for complaints. Dr Skiendzielewski's initial contact with the residency review committee, although very brief, turned out to be positive for him. His judgment, however, in m y opinion, was arrived at in haste, was not entirely fair, and was expressed in a hyperbole that I, for one, do not expect from a director of a residency program in emergency medicine.
George Podgorny, MD, Chairman RRC-EM
To the Editor: Dr Skiendzielewski's point is well taken. Those of us who were active in the Liaison Residency Endorsement Committee recognized many imperfections in our endorsement process, but an indubitable strength was survey by physician peers - - a parallel to jury-by-peers. The closer and more familiar a surveyor to the scene at hand, the greater likelihood of a sophisticated and penetrating survey. The use of non-physician and non-specialty surveyors has been roundly criticized in other specialty organizations - - most particularly Surgery. Although there may be good reasons for the current use of non-physician, non-emergency-medicine surveyors, I agree with Dr Skiendzielewski that this practice should be carefully reviewed by the Residency Review Committee on Emergency Medicine. Robert H. Dailey, MD Past-Chairman Liaison Residency Endorsement Committee
Pressures During Manual and Mechanical CPR To the Editor: The article by McDonald, entitled "Systolic and Mean Arterial Pressures During Manual and Mechanical CPR in H u m a n s " {11:292-295, June 1982) is interesting, but presents several problems. First, the data presented do not justify the conclusion that, "Chest compression by a pneumatic device is superior . . . in producing higher mean arterial pressures (MAP)." A straightforward two-tailed test for a significant difference between the MAP data groups obtained with manual versus mechanical CPR reveals the following: 12:4 April 1983
Manual Mean = 24.9 m M Hg SD = 1 3 . 8 m M H g
Mechanical Mean = 31.9 m M Hg SD = 1 3 . 7 m M H g
with 28 degrees of freedom, t = 1.34. The probability that the two groups are not different is considerably greater than 10% (P > .1). Thus the null hypothesis that the two data groups represent random sampling from the same data pool is not excluded, and the difference is not statistically significant.
Annals of Emergency Medicine
267/115
CORRESPONDENCE
Second, the fact that there was zero survival in the series is troublesome. These outcome data can hardly be used to recommend either prolonged mechanical or m a n u a l CPR. Indeed, the fatal flaw m a y lie in prolonged closed chest CPR rather than in either the T h u m p e r ® or the hand. The ratio of live discharges to the n u m b e r of CPRs initiated outside the hospital varies from 5% to 20%. 1-s This n u m b e r includes patients w i t h p e r m a n e n t neurologic injury, and therefore the neurologically intact discharge rate is still lower. Bergner et al t have reported progressively poor outcome when definitive resuscitation (defibrillation) occurred more than six m i n u t e s following collapse, even w i t h immediate CPR initiation. Three series of patients w i t h prolonged CPR following rapid initiation of ALS were reported at the UAEM m e e t i n g last year. 6a Total patients in the pooled data from these series are 392. Of these, 88 were successfully resuscitated. Only 14 patients were discharged neurologically intact. Similar trends indicating very little cardiac or cerebral protection by early but prolonged CPR are also evident in the reports from Eisenberg. 4 Evidence is accumulating that the physiology involved in closed chest CPR m a y be responsible for the poor outcome data we are now forced to confront. The systolic arterial pulse produced by CPR is a result of elevated intrathoracic pressure, not ventricular compression. 9-1° Thus there is little t h o r a c i c a r t e r i o v e n o u s p e r f u s i o n p r e s s u r e gradient. N i e m a n n et al tl have recently reported the poor net coronary perfusion pressures. We have done cerebral cortical perfusion studies in dogs during CPR (mean systolic pressure = 75 m M Hg) demonstrating less than 10% of prearrest flow (.732 -+ .3 c c / m i n / g m vs .054. -+ .01 cc/min/gm) in the cerebal cortex with i m m e d i a t e initiation of CPR. t2 Kohler et a113 have reported similar data. Bircher and Safar 14 also have reported these low flows and demonstrated little improvement w i t h the so-called " n e w " CPR or abdominal binding. In contrast, cerebral cortical blood flow during internal cardiac massage is equal to or greater than prearrest perfusion, is This reflects substantially better cardiac output, as previously reported in patients, ~6 and also the production of arterial pressure by ventricular ejection without simultaneous massive elevation of thoracic venous pressures. Finally, the argument that the poor perfusion pressure and low flows generated by CPR are better than nothing can no longer be accepted uncritically. H o s s m a n n and Kleihues ~z and Nordstrom et al TM have studied brain no flow versus 10% flow. The data demonstrate a tenfold greater neuronal lactate accumulation and m u c h poorer ATP recovery with 10% flow. Mitochondrial injury is also exacerbated in the low flow m o d e ) 9 Thus the McDonald paper demonstrates low MAPs during CPR without any significant difference between m a n u a l and mechanical CPR. It does not report simultaneous CVPs, and thus net perfusion pressures cannot be discussed. It does provide another small series confirming the statistical futility of prolonged CPR. In this respect it serves to raise the issues reviewed here. In view of these issues revolving around CPR itself, further studies of " T h u m p e r ® vs pumper" would appear to have low priority at this time. 116/268
Blaine C. White, MD Department of Emergency Medicine Michigan State University East Lansing Carl D. Winegar, MD Paul J. Hoehner Raymond Jackson, MD Department of Emergency Medicine Detroit Receiving Hospital Detroit Kathleen Joyce, MD Department of Anesthesia Sinai Hospital Detroit 1. Bergner L, Eisenberg M, Hallstrom A, et al: Evaluation of paramedic services for cardiac arrest. US Department of Health and Human Services, National Center for Health Services Research Report (HS 02456), December 1981. 2. Eliastam M, Duralde T, Martinez F, et al: Cardiac arrest in the EMS system: Guidelines for resuscitation. JACEP 6:525-529, 1977. 3. Myerberg RJ, Kessler KM, Zaman L, et al: Survivors of prehospital cardiac arrest. JAMA 247:1485-1490, 1981. 4. Eisenberg MS, Copass MK, Hallstrom A: Management of out-ofhospital cardiac arrest - - Failure of basic EMT services. JAMA 243:1049-1051, 1980. 5. Nagel EL, Liberthson RR, Hirschman JC, et al: Emergency care. Circulation 52(Suppl 3):216, 1975. 6. Mahoney BD, Mirick MJ: Efficacy of pneumatic trousers in refractory prehospital cardiopulmonary arrest. Ann Emerg Med 12:812, 1983. 7. Campell DB, Hurvitz S, Hammon B, et al: Field vs emergency department resuscitation of out-of-hospital cardiac arrest. Presented at the UAEM Scientific Meeting, Salt Lake City, Utah, April 15-17, 1982. 8. Mirick MJ, Mahoney BD, Sherman R, et al: Refractory prehospital cardiac arrest: A contrast from previously reported prognostic indicators. Presented at the UAEM Scientific Meeting, Salt Lake City, Utah, April 15-17, 1982. 9. Rudikoff MT, Maughan WL, Effron M, et al: Mechanisms of blood flow during CPR. Circulation 61:345-352, 1980. 10. Niemarm JT, Rosborough JP, Haus Knecht M, et al: Pressure synchronized cineangiographic observations during experimental CPR. Circulation 64:985-991, 1981. 11. Niemann JT, Rosborough JP, Ung S, et al: Coronary perfusion pressure during experimental CPR. Ann Emerg Med 11:127-131, 1982. 12. Jackson R, Danosi S, White BC: Cerebral cortical perfusion during CPR and post-resuscitation: Presented at the International Scientific Symposium on Cerebral Resuscitation, Detroit, Michigan, July 7-8, 1982. 13. Kohler RC, Chandra N, Guerci AD, et al: Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding following cardiac arrest in dogs. Circulation (in press). 14. Bircher N, Safar P: Comparison of standard and "new" dosed chest CPR and open-chest CPR in dogs. Crit Care Med 9:384, 1981. 15. Joyce K, Vigor D, White BC: Perfusion of the cerebral cortex by
Annals of Emergency Medicine
12:4 April 1983
internal cardiac massage alter a 15-minute cardiac arrest in dogs. Presented at the International Scientific Symposium on Cerebral Resuscitation, Detroit, Michigan, July 7-8, 1982. 16. Del Guercio LRM, Feins NR, Cohn JD, et al: Comparison of blood flow during external and internal cardiac massage in man. Circulation 31-32(Suppl 1):I-171-I-180, 1965. 17. Hossman KA, Kleihues P: Reversibility of ischemic brain damage. Arch Neurol 29:375-382, 1973. 18. Nordstrom CH, Rehncrona S, Siesjo BK: Restitution of cerebral energy state after 30 minutes of complete ischemia in rats anesthetized with nitrous oxide or phenobarbital. J Neuroclhem 30:479-486, 1978. 19. Rehncrona S, Mela L, Siesjo BK: Recovery of brain mitochondrial function in the rat after complete and incomplete cerebral ischemia. Stroke 10:437-446, 1979.
To the Editor: We believe White et al have erred in their choice of a statistical method to help t h e m in their interpretation of our data. They have done an analysis using the two-tailed test for equality of two means. The use of this method, in this situation, is incorrect because the two sets of data w h i c h make up the samples are not independent. This is so because both sets of readings, manual vs mechanical, were t a k e n from the same set of patients. Furthermore they have Incorporated into their statistical treatment the large differences in pressures generated from patient to patient. Our study design eliminated the need to consider these differences, which are not pertinent. W h a t we did was to analyze data derived from the comparison of pressures obtained from matched pairs. 1 These m a t c h e d pairs are pressures generated in the same person by 1) mechanical and 2) manual chest compression. This is t e r m e d a "randomized block design." The appropriate test is the paired difference test. W i t h 14 degrees of freedom we obtained a t of - 2.84. The difference is statistically significant (P < .01), which justifies our excluding the null hypothesis. W h i t e et al further state that zero survival is troublesome. Our paper stated that all 15 persons were in the late stages of the resuscitative effort and, furthermore, that the data presented did not represent our typical experience in generating m e a n arterial pressures (MAPs) in persons who are in the early stages of the resuscitative process. Such persons were, by design, eliminated from our study because so m a n y other t r e a t m e n t modalities are typically utilized early in resuscitative efforts which could affect the pressures during the study and thus render the comparison invalid. To say that we r e c o m m e n d either prolonged mechanical or manual CPR is not correct. In our paper we clearly state that on m a n y occasions systolic arterial pressures which might be interpreted as consistent with continued brain survival were associated w i t h MAPs so low as to preclude the possibility of survival. This was true not only for some patients undergoing m a n u a l chest compression, but in some of those undergoing mechanical chest compression as well. 12:4 April 1983
What we intended to i m p l y was that in such instances, unless maneuvers could be accomplished to increase MAP w i t h i n a very short period of time, the resuscitative efforts should be discontinued. We are aware of the study of N i e m a n n et al ~ which indicates the poor net coronary perfusion pressure during closed chest CPR. We were not aware of this fact at the time the study was being performed. We are n o w s i m u l t a n e o u s l y measuring central venous and central arterial pressures during some of our resuscitative efforts. We have no disagreement w i t h the elaboration of the extremely poor results attendant to prolonged CPR. However, even with prolonged CPR, survival is greater than zero. And any technique which increases the rate of survival by even a small factor is worthwhile. We believe that our study indicates that u t i l i z a t i o n of m e c h a n i c a l chest compression, together w i t h rapid i m p l e m e n t a t i o n of MAP monitoring, can lead to a more sophisticated resuscitative effort. This could, in turn, lead to an increased rate of survival. Most studies emanate from large hospitals and teaching institutions which have available to t h e m at the time of resuscitation large n u m b e r s of h i g h l y skilled personnel. However, the vast preponderance of cardiac arrests occur in the prehospital care setting, in small emergency departments, and in critical care units in which only one or two people are available to perform the resuscitation. The use of a m e c h a n i c a l device to both compress the chest and to ventilate frees up the hands to perform other critically important tasks and, perhaps more important, flees up the m i n d to do decision m a k i n g w h i c h is of higher quality. The other points raised in the reply to our paper, we believe, are not so m u c h questions regarding our study but more a discourse on the current pattern of research being done by White's group and by others. We look forward enthusiastically to the results of these studies, and stand ready to change our methods when it is scientifically sound to do SO.
In summary, we believe our study does demonstrate that mechanical chest compression results in higher MAPs and could result in increased survival. Furthermore, we continue to urge those persons who are performing resuscitations and who have access to m o n i t o r i n g equipment to rapidly i m p l e m e n t MAP m e a s u r e m e n t early on in their resuscitative efforts. In closing, we agree w i t h White et al that further studies of " ' T h u m p e r ® vs pumper' appear to have a low priority" at this time. Instead, we should all be performing studies which will elucidate better methods of performing resuscitations so that we can increase the current miserably low rate of survival. John L. McDonald, M D Santa Rosa, California 1. Mendenhall W: Introduction to Probability and Statistics, ed 3. Belmont, CA, Duxbury Press, 1971, p 1035-1039. 2. Niemarm AP, Rosborough JP, Ung S, et al: Coronary perfusion pressure during experimental CPR. Ann Emerg Med 11:127-131, 1982.
Annals of Emergency Medicine
269/117