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Aortic and right atrial pressures during standard and simultaneous compression and ventilation cpr in human beings
oRIGINAL CONTRIBUTION cPR, aortic and atrial pressures during
Aortic and Right Atrial Pressures During Standard and Simultaneous Compression and Ventilation CPR in Human Beings Coronary perfusion pressure, as reflected by the diastolic aortic to right atrial (Ao-RA) pressure gradient, has been shown to correlate well with coronary blood flow during standard external CPR (SE-CPR) and is an important determinant of successful cardiac resuscitation. Few studies have documented such Ao-RA gradients in human beings, however. Twenty patients sustaining out-of-hospital cardiopulmonary arrests and basic cardiac life support were instrumented with thoracic aortic and right atrial catheters on arrival in the emergency department. The mean time from arrival in the ED to catheter placement was 16.5 +- 6.0 minutes. With SE-CPR, peak systolic aortic and right atrial pressures were 73.7 + 20.2 m m Hg and 69.6 + 18.3 m m Hg, respectively. End diastolic aortic and right atrial pressures were 27.9 + 7.3 m m Hg and 20.3 + 7.2 m m Hg, respectively, with an end diastolic gradient of 7.9 + 9.1 m m Hg. Three patients had systolic Ao-RA gradients of more than 25 m m Hg, which is consistent with some cardiac compression as a mechanism of flow. Five patients also had one-minute trials of simultaneous compression and ventilation CPR (SCV-CPR). Ao-RA end diastolic gradients decreased in four of the five during SCV-CPR. No patient in this study was resuscitated successfully. We conclude that ED SECPR provides little coronary perfusion for victims of prehospital carddiac arrest. Although SCV-CPR has been shown to improve carotid blood flow in human beings, it appears to have an adverse effect on the already minimal myocardial perfusion provided by SE-CPR. [Martin GB, Carden DL, Nowak RM, Lewinter JR, Johnston W, Tomlanovich MC: Aortic and right atrial pressures during standard and simultaneous compression and ventilation CPR in human beings. Ann Emerg Med February 1986;15:125-130.]
Gerard B Martin, MD Donna L Carden, MD Richard M Nowak, MD, FACEP Jody R Lewinter, MD William Johnston, MD Michael C Tomlanovich, MD, FACEP Detroit, Michigan From the Department of Emergency Medicine, Henry Ford Hospital, Detroit, Michigan. Received for publication May 28, 1985. Revisions received August 28, 1985. Accepted for publication September 26, 1985. Presented at the University Association for Emergency Medicine Annual Meeting in Kansas City, Missouri, May 1985. Address for reprints: Gerard B Martin, MD, Department of Emergency Medicine, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, Michigan 48202.
INTRODUCTION Recent investigations of CPR have helped to elucidate mechanisms of blood flow and to document the poor regional perfusion that occurs. Although evidence generated by Rudikoff, 1 Niemann, 2 and others3, 4 has provided convincing support for the "thoracic pump" mechanism of flow, the relative role of direct cardiac compression remains unresolved, s-7 Methods of CPR that exploit the thoracic pump mechanism, such as simultaneous compression and ventilation CPR (SCV-CPR) and abdominal binding, have been shown to increase carotid flow,S,9 but have had variable effects on coronary blood flow.S-ll Although adequate myocardial perfilsion is essential for successful resuscitation 12, standard external CPR (SE-CPR) provides little coronary blood flow to the fibrillating myocardium.le, u,~3,14 During CPR in the animal model, coronary blood flow has been shown to correlate with the coronary peffusion pressure, as reflected by the diastolic aortic to right atrial (Ao-RA) pressure gradient 12,13,~s and with the diastolic aortic pressure aloneA6,17 Successful resuscitation also has been related directly to these pressures.lZ, lS 21 Most of these data have been obtained from animal models. The obvious differences between these models and the person with cardiac arrest, as well as the lack of clinical studies during resuscitation, suggest that caution be used in extrapolating these data to human beings. Although it long has been known that pressure does not necessarily indicate flow during CPR 22-24, important information may be obtained from pressure monitoring during CPR, The purpose of our investigation was to 15:2 February 1986
Annals of Emergency Medicine
125/37
ATRIAL PRESSURES Martin et al
determine the feasibility of monitoring aortic (Ao) and right atrial (RA) pressures in h u m a n beings during SECPR and SCV-CPR and to attempt to apply concepts recently developed in the animal model to the h u m a n being.
METHODS Patients with out-of-hospital cardiac arrest brought to the Henry Ford Hospital emergency department were considered for inclusion in the study if a m e m b e r of the research t e a m was present. Patients with obvious significant disease of other than cardiovascular etiology and patients w i t h prol o n g e d d o w n t i m e s were excluded. Because there was only a single adv a n c e d cardiac life support (ACLS) unit in the city of Detroit, all patients received only basic cardiac life support prior to arrival in the ED. On arrival, ACLS protocol was instituted immediately, i n c l u d i n g 1-mg doses of epinephrine every five minutes and intub a t i o n . S o d i u m b i c a r b o n a t e was administered as necessary to maintain arterial pH at more than 7.2. SE-CPR was performed using a mechanical chest compressor and ventilator (Thumper% Michigan Instruments, Grand Rapids, Michigan) with sufficient force to compress the chest 2.5 to 3 inches (80 to 100 pounds of force). Ventilation pressures were set at 30 cm H20. A 7-F, 25-cm radiopaque double lumen catheter (Cook Incorporated, Bloomington, Indiana) was inserted percutaneously into the subclavian vein and advanced to the RA. The proximal port was used for drug administration and the distal port for pressure m o n i t o r i n g . P e r c u t a n e o u s placement of a 5.8-F, 90-cm radiopaque catheter (Cook Incorporated) into the thoracic aorta using a guide wire technique through the femoral artery then was attempted. The length of catheter necessary for proper placement was estimated prior to insertion. T h e c a t h e t e r s were c o n n e c t e d to Gould Statham P-50 transducers, and simultaneous pressure tracings were recorded using Hewlett-Packard 78205D amplifiers and a H e w l e t t Packard 7758 multichannel recorder. Both transducers and fluid flush systems were set up and calibrated prior to the patient's arrival in the ED. In addition to SE-CPR, five patients also had trials of SCV-CPR as described by Chandra. 2s SCV-CPR was performed using a specially modified computerized Thumper ® at a rate of 38/126
TABLE 1. Mean values for initial pressures*
Systolic Diastolic
Aortic
Right Atrial
Ao-RA
73.7 _+ 20.2
69.6 ___ 18.3
4.1 +- 13.2
27.9 +_ 7.3
20.3 _+ 7.2
7.9 +
9.1
*All values in mm Hg.
TABLE 2. Systolic pressures for three patients with systolic Ao-RA gradients
of more than 25 m m Hg*
Aortic
Right Atrial
Patient No. 1
115.2
88,2
Ao-RA 27
Body Habitus
Patient No. 2
93.5
68.0
25.5
Stocky
Patient No. 3
62.6
36.8
25.8
Thin
Thin
*All values in mm Hg.
40 cycles per minute, ventilation pressure of 100 cm H20, and 60:40 compression to relaxation ratio. In patients receiving only SE-CPR, pressures were measured for one-minute intervals every two to five minutes during the resuscitation. In the patients receiving SCV-CPR, one-minute trials of SCV-CPR were alternated with SE-CPR every two to four minutes. In accordance w i t h guidelines specified by the H u m a n Investigation C o m m i t t e e at Henry Ford Hospital, SE-CPR was reinstituted if pressures decreased during SCV-CPR. Reported pressures represent the m e a n of 20 consecutive readings. Pressures measured during chest compression were considered systolic, and those during relaxation, diastolic. Aortic and RA systolic pressures were measured at peak levels, and all diastolic pressures were recorded at end-diastole. Supine chest radiographs were taken in all patients at the conclusion of resuscitation to assess catheter position. Differences in intravascular pressures were assessed using p a i r e d . t tests with P < .05 considered significant. All m e a n pressures are noted with standard deviations. RESULTS Data were analyzed from 20 of the 23 patients originally entered in the study. Two patients were excluded because of i m p r o p e r a o r t i c c a t h e t e r placement (the extrathoracic subclavian artery in one and the abdominal Annals of Emergency Medicine
aorta in the other). The femoral artery could not be cannulated in one patient. The study included 12 w o m e n and eight m e n with a m e a n age of 61.7 + 16.0 years. No patient was resuscitated successfully. The time from collapse until arrival in the ED was not available in two cases, but averaged 18 + 8 minutes in the remaining patients. The mean time from arrival in the ED until the first pressure tracings were obtained was 16.5 +_ 6 minutes. Initial r h y t h m s included ventricular fibrillation in ll, pulseless i d i o v e n t r i c u l a r r h y t h m in six, and asystole in three. Mean values for the initial pressures from all patients are shown (Table 1). The range for diastolic Ao-RA gradients was from -14.4 to 21.4 m m Hg, including five patients with initial diastolic Ao-RA gradients of less than 0. Although mean Ao and RA systolic pressures were not significantly different (P > .05), three patients had systolic Ao-RA gradients of more than 25 m m Hg (Table 2). Two of these had a t h i n body habitus; however, n o t all t h i n p a t i e n t s s h o w e d this systolic pressure difference. R e p r e s e n t a t i v e tracings are shown (Figures 1A and 1B). The initial systolic RA pressure was 28.9 m m Hg more than Ao in one patient. This initial difference may have been secondary to massive aspiration rather than cardiac compression because subsequent systolic pressure differences after oxygenation and suctioning were minimal (Figures 2A and 15:2 February1986
A 100
100 mm Hg
mm Hg
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j~, 'Ao ,RA /'~
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2B). Not all patients w h o aspirated had large negative Ao-RA systolic gradients. The other three patients with systolic Ao-RA gradients of more than 25 m m Hg maintained this difference on subsequent readings as long as 20 minutes later. Thirteen patients had at least two readings separated by nine minutes or more and were assessed to determine changes in diastolic Ao-RA gradients over time. The gradient increased in five patients, decreased in three, and remained essentially u n c h a n g e d (___ difference ~ 2 m m Hg) in five (P > .05). The mean change was an increase of 1 --- 9 m m Hg, with the changes ranging from a decrease of 20.3 m m Hg to an Increase of 14.3 m m Hg. The m e a n t i m e b e t w e e n readings was 17.2 +_ 7 m i n u t e s , w i t h a range of nine to 27 minutes. There did not appear to be any consistent improvem e n t in diastolic A o - R A gradients after epinephrine administration. Aortic and RA pressures for the five patients receiving SCV-CPR in addition to SE-CPR are shown (Table 3). Although the diastolic gradient decreased in four of the five patients during SCV-CPR, the mean decrease of 3.6 +_ 4.0 m m Hg was not statistically significant (P > .05). The m e a n increase in Ao systolic pressure w i t h SCV-CPR was 2.3 _+ 9.4 m m Hg and also was not statistically significant (P > .05). These data compare only the initial minute of SCV-CPR with the preceding tracing of SE-CPR. The 0nly 15:2 February 1986
patient to show an increase in diastolic Ao-RA gradient with SCV-CPR was the same patient noted earlier to have massive aspiration. This patient had an initial i m p r o v e m e n t in diastolic gradient from 11.5 m m Hg to -8.3 m m Hg with SCV-CPR. During a final trial of SE-CPR five m i n u t e s later, the gradient increased further to 0 m m Hg (Figure 2B). The other four patients underwent at least two comparisons of SCV-CPR and SE-CPR and showed a significant decrease in diastolic Ao-RA gradients of 5.1 + 2 m m Hg with SCV-CPR (P < .01). There was an increase in systolic Ao pressure of 3.0 +- 10.2 m m Hg, but this was not significant (P > .05). T h e diastolic A o - R A gradient showed a large decline over time with SCV-CPR in two patients with multiple comparisons. The gradient during SE-CPR was better sustained in these patients. For example, one patient had a decrease in diastolic Ao-RA gradient of 5.5 m m Hg over a 27-minute period with SE-CPR, compared to a drop of 16.2 m m Hg with SCV-CPR (Table 4).
DISCUSSION The rationale for using the coronary perfusion pressure (CPP), as estimated by the diastolic A o - R A gradient, as an index of coronary blood flow has b e e n e s t a b l i s h e d in t h e a n i m a l model.X2A3, Is A l t h o u g h few studies have measured this gradient In h u m a n beings, it is feasible as evidenced by our success rate of 87%. McDonald Annals of Emergency Medicine
FIGURE 1. Samples of actual tracings
obtained during CPR in two patients. A o - R A is the subtraction circuit providing continuous tracings of AoRA gradient. A. Patient showing evidence for the thoracic pump mechanism with near equality of Ao and RA systolic pressures. B. Patient showing evidence of cardiac compression with Ao-RA systolic gradients of approximately 27 m m Hg. FIGURE 2. Tracings from patient with massive aspiration. A. Initial tracings show large negative systolic and diastolic gradients. B. Tracings obtained ten minutes later show resolution of negative gradients and equality of systolic and diastolic Ao and RA pressures. has reported two six-patient series of p a r a m e d i c - t r e a t e d , refractory, prehospital cardiac arrests. In the first series, 26 diastolic gradients were less than 7 m m Hg in four cases. One patient had a gradient of 11 m m Hg, and another with a 16-mm-Hg CPP gradient was a l o n g - t e r m survivor. In McDonald's most recent series, 2z the C.PP a v e r a g e d 5.2 + 3.0 m m Hg. Sanders zs reported six p a t i e n t s in w h o m radial a r t e r y rather than Ao pressure was m o n i t o r e d along with central venous pressure, and he noted a mean diastolic gradient of 1 m m Hg. Howard 29 has monitored central venous and thoracic aortic pressures in 14 127/39
ATRIAL PRESSURES Martin et al
patients undergoing both SE-CPR and interposed abdominal compression CPR. A m e a n gradient of 2.6 m m Hg was obtained during SE-CPR. Our reported diastolic Ao-RA gradient of 7.9 + 9.1 m m Hg is higher than previously reported, b u t still is low w h e n compared to experimentally determined m i n i m u m perfusion press u r e s . D o w n e y , u s i n g an i s o l a t e d f i b r i l l a t i n g h e a r t model, has s h o w n pressure gradients of 18 m m Hg and 28 m m Hg to be necessary for subepicardial and subendocardial flow, respectively.30 These values are not dir e c t l y a p p l i c a b l e to t h e ED p a t i e n t because they were obtained in unobstructed, m a x i m a l l y dilated coronary arteries. In a study of 14 dogs undergoing CPR, N i e m a n n 19 found a diastolic A o - R A gradient of 18 m m Hg to be predictive of successful defibrillation. In another study, he found a significant difference between Ao-RA grad i e n t in survivors (23 + 6 m m Hg) and nonsurvivors {10 + 7 m m Hg). ~o R a l s t o n 12 r e p o r t e d a m i n i m u m gradient of 15 m m Hg necessary for resuscitation and short-term survival. In spite of their limitations, these pressures are of some use in setting minim u m coronary perfusion pressure requirements. A o r t i c diastolic pressure alone has been shown to correlate w i t h coronary blood flow16,17 and successful resuscitation.2O, ~1 R e d d i n g 18 s h o w e d t h a t w h e n Ao diastolic pressure could be raised to 40 m m Hg, dogs were resuscitated successfully from asphyxial arrest. Resuscitation was unsuccessful if this m i n i m u m d i a s t o l i c p r e s s u r e was not achieved. The aortic diastolic pressure of 27.9 + 7.3 m m Hg noted in our study falls below the m i n i m u m of 40 m m Hg set b y Redding, b u t above t h e 22 m m Hg n e c e s s a r y for successful defibrillation noted by N i e m a n n . 2o A l t h o u g h caution m u s t be used in extrapolating these n u m bers derived from animals to ED patients w i t h coronary artery disease, it is clear t h a t SE-CPR provides l i t t l e myocardial perfusion. T h e r e were no s u r v i v o r s in o u r study despite the fact that 11 patients p r e s e n t e d in v e n t r i c u l a r f i b r i l l a t i o n . There are three reasons for this high mortality. Most important is the prolonged downtime prior to institution of ACLS measures. C u m m i n g s 31 recently has shown that ACLS m u s t be instituted within ten to 12 m i n u t e s of collapse to be effective. Second, pa-
40/128
TABLE 3. Mean values for initial pressure readings in patients having both
SE-CPR and SCV-CPR*
Aortic Right Atrial Ao-RA Type of CPR (Systolic/Diastolic) (Systolic/Diastolic) (Systolic/Diastolic) SE-CPR
88.4 + 29.2 28.1 _+ 9.1
86.2 + 18.9 17.5 _+ 9.3
2.2 + 19.9 10.5 + 13.3
SCV-CPR
90.7 + 24.9 24.4 _+ 13.4
88.6 + 13.4 17.4 _+ 10.0
5.7 + 17.3 6.9 -+ 10.2
*All values in mm Hg,
tients who were resuscitated successfully were defibrillated soon after arrival in the ED, prior to the placement of the Ao and RA lines. Third, the gradients obtained with SE-CPR were far below e s t i m a t e d m i n i m u m coronary p e r f u s i o n p r e s s u r e r e q u i r e m e n t s . If Ao-RA gradients are valid indicators of coronary perfusion, successful resuscitation would not be expected in these patients. The lack of survivors m a y l i m i t the interpretation of this study, however. If Ao-RA gradients are not valid indicators of myocardial perfusion, survival m a y be possible w i t h low gradients. This possibility cannot be excluded w i t h the current data. As noted, five patients had initial Ao-RA gradients of less than 0, implying retrograde flow of venous blood through the coronary circulation. Such negative coronary perfusion pressures have been noted by McDonald 26 and Sanders. 28 Although the exact significance of negative perfusion pressures remains to be determined, it is probably associated w i t h perfusion of the m y o c a r d i u m w i t h deoxygenated venous blood and a nonresuscitatable heart. Initial theories on the m e c h a n i s m of flow during CPR presumed that the heart was compressed against the stern u m , l e a d i n g t o t h e e j e c t i o n of blood. 3~ More recent data have provided a convincing argument for the t h o r a c i c p u m p as a m e c h a n i s m of flow.l, a A c c o r d i n g to t h i s t h e o r y , global increases in intrathoracic pressure cause blood flow with the heart acting merely as a conduit. Equalization of systolic pressures in the RA and Ao, as seen in the majority of patients in our study, provides evidence supporting the thoracic p u m p mechanism of flow. Although other limited human data support the thoracic p u m p theory,g, 4 the three patients in
Annals of Emergency Medicine
our s t u d y w i t h s y s t o l i c A o - R A gradients of more than 25 m m Hg presumably had cardiac compression contributing to flow. In the presence of cardiac compression, one w o u l d exp e c t t h e large s y s t o l i c A o - R A gradients as seen in these patients, g3 Two of these three patients were small and thin-chested, a body habitus more l i k e l y to lend itself to cardiac compression. 6 The 15% of patients w i t h e v i d e n c e of cardiac c o m p r e s s i o n in our study compares favorably w i t h the 30% proposed by Rudikoff. 1 In Chandra's original study of SCVCPR in h u m a n beings, there was a significant increase in m e a n systolic radial artery pressure from 40.6 to 53.1 m m Hg. 2s M c D o n a l d , 27 h o w e v e r , found a decrease in systolic pressures from 112 + 7.3 to 93 + 8.1 m m Hg. O u r d a t a s h o w no s i g n i f i c a n t difference between the two techniques. The reason for the discrepancy in results is not clear. T h e small sample size a n d large v a r i a n c e in s y s t o l i c pressures are l i m i t i n g factors in our study. C o r o n a r y blood flow d u r i n g SCVCPR in the a n i m a l m o d e l has been shown to either increase minimally8,10,16 or r e m a i n t h e s a m e . n Sanders 34 was u n a b l e to r e s u s c i t a t e any dogs that received SCV-CPR w i t h a b d o m i n a l b i n d i n g , b u t five of six dogs t h a t had SE-CPR were resuscitated successfully. A significantly l o w e r A o d i a s t o l i c a n d A o - R A dia s t o l i c p r e s s u r e g r a d i e n t w e r e prop o s e d as p o s s i b l e r e a s o n s for t h e failure. Babbs, 6 however, found coron a r y p e r f u s i o n p r e s s u r e to be unchanged with SCV-CPR in a series of 12 dogs. Survival was not addressed in this study. Niemann19 found survival as well as Ao-RA gradients to be increased in animals receiving SCV-CPR with
15:2 February 1986
T A B L E 4. A o - R A diastolic gradients comparing SE-CPR w i t h SCV-CPR over time*
SE
SCV
SE
CPR Type SE SCV
SE
SCV
SE
Time after arrival in ED (min)
10
12
14
17
19
34
36
37
Ao-RA diastolic (mm Hg)
21.4
18.3
25.6
21.3
13.4
15.9
2.1
15.9
*This patient demonstrates a decrease in gradient of 5.5 mm Hg with SE-CPR, compared to a decrease of 16.2 mm Hg with SCV-CPR during the same period.
pneumatic vest and binder when comp a r e d t o SE-CPR. M c D o n a l d 2z reported a m i n i m a l increase in coronary perfusion pressure from 3 m m Hg to 3.4 m m Hg w i t h SCV-CPR in five patients. Although our readings for initial d i a s t o l i c A o - R A g r a d i e n t s were not significantly different w i t h SCVCPR, the patient w i t h aspiration mentioned previously does skew the results. W h e n f u r t h e r trials w i t h t h e other four patients were analyzed, a statistically significant decrease w i t h SCV-CPR was found. It m u s t be emphasized that although this decrease in diastolic Ao-RA gradients is numerically significant, it may not be clinically significant. SCV-CPR in our experience, however, does not improve CPP and m a y well have an adverse effect on this important index of coronary blood flow. Thus, although SCVCPR m a y lead to improved neurological recovery by virtue of its increasing cerebral blood flow, could it ultimately decrease survival by decreasing coronary blood flow? Further h u m a n studies with large numbers of patients are needed to address this question. Few studies have addressed the duration of CPR as it relates to organ flow. Sharff 3s found a significant decrease in blood flow to the heart and brain at ten m i n u t e s of CPR compared to two minutes. There was no consistent decline in diastolic Ao-RA gradients w i t h t i m e in our study. In fact, several patients showed m a r k e d improvement in their gradients. Improvement m a y have been related to catecholamine administration, correction of acidosis, adequate oxygenation, or other factors n o t y e t identified. In Some patients, the vasculature m a y be more r e s p o n s i v e to t h e r a p y d u r i n g prolonged CPR than previously t h o u g h t . In a.ddition, t h e s p e c i f i c cause of cardiac arrest was not verified by autopsy and m a y have had an effect on C P R h e m o d y n a m i c s and the 15:2February 1986
changes w i t h t i m e and therapy. Diastolic Ao-RA gradients seemed to be better maintained over time w i t h SECPR t h a n w i t h SCV-CPR (Table 4). The reason for this effect is not clean CONCLUSION Invasive monitoring of Ao and RA p r e s s u r e s in t h e ED is feasible and m a y yield clinically valuable information to guide resuscitation efforts. ED SE-CPR provides little CPP for vict i m s of out-of-hospital cardiac arrest, with clinically obtained pressures m u c h below m i n i m u m requirements derived from animal models. Although SCV-CPR m a y improve cerebral b l o o d flow, e v i d e n c e f r o m t h i s l i m i t e d s t u d y suggests t h a t it m a y have an adverse effect on the already m i n i m a l m y o c a r d i a l p e r f u s i o n provided by SE-CPR. Further studies in h u m a n beings are needed to examine diastolic Ao-RA gradients during CPR to define their prognostic importance a n d r e s p o n s i v e n e s s to t h e r a p e u t i c modalities, including "new" techniques of CPR. The authors acknowledge the tireless efforts of Ms Marty Racey in the preparation of this manuscript.
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assessment of heart chamber size and valve motion during cardiopulmonary resuscitation by two-dimensional echocardiography. A m Heart J 1981;102:368-373. 5. Babbs CF: New versus old theories of blood flow during CPR. Crit Care Med 1980;8:191-195. 6. Babbs CE Tacker WA, Paris RL, et al: CPR with simultaneous compression and ventilation at high airway pressure in four animal models. Crit Care Med 1982;10: 501-504. 7. Maier GW, Tyson GS, Olsen CO, et al: The physiology of external cardiac massage: High-impulse cardiopulmonary resuscitation. Circulation 1984;70:86-101. 8. Chandra N, Weisfeldt ML, Tsitlik J, et al: Augmentation of carotid flow during cardiopulmonary resuscitation by ventilation at high airway pressure simultaneous with chest compression. A m J Cardiol 1981;48:1053-1063. 9. Niemann JT, Rosborough JP, Ung S, et al: Hemodynamic effects of continuous abdominal binding during cardiac arrest and resuscitation. A m J Cardiol 1984;53: 269-274. 10. Luce JM, Ross BK, O'Quin RJ, et al: Regional blood flow during cardiopulmonary resuscitation in dogs using simultaneous and non simultaneous compression and ventilation. Circulation 1983;67: 258-265. 11. Koehler RC, Chandra N, Guerci AD, et ah Augmentation of cere~oral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs. Circulation 1983;67:266-275. 12. Ralston SH, Voorhees WE), Babbs CF: Intrapulmonary epinephrine during prolonged cardiopulmonary resuscitation: Improved regional blood flow and resuscitation in dogs. A n n Emerg Mect 1984; 13:79-86. 13. Ditchey RV, Winkler JV, Rhodes CA: Relative lack of coronary blood flow during dosed-chest resuscitation in dogs. Circulation 1982;66:297-302. 14. Bellamy RF, DeGuzman LR, Pedersen DC: Coronary blood flow during cardio129/41
ATRIAL PRESSURES Martin et al
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31. Cummings RO, Eisenberg MS, Hallstrom AP, et al: Survival of out-of-hospital cardiac arrest with early initiation of cardiopulmonary resuscitation. Am ] Emerg Med 1985;3:114-118.
25. Chandra N, Rudikoff M, Weisfeldt ML: Simultaneous chest compression and ventilation at high airway pressure during cardiopulmonary resuscitation. Lancet 1980;1:175-178.
32. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closed chest cardiac massage. JAMA 1960;173:1064-1067.
26. McDonald JL: Coronary perfusion pressure during CPRin human beings {abstract). Ann Emerg Med 1983;12:144.
33. Niemann JT, Rosborough JP, Hausknecht M, et al: Blood flow without cardiac compression during CPR. Crit Care Med 1981;9:380-381.
27. McDonald JL: Effect of interposed abdominal compression during CPR on central arterial and venous pressures. A m J Emerg Med 1985;3:156-159.
34. Sanders AB, Ewy GA, Alferness CA, et al: Failure of one method of simultaneous chest compression, ventilation and abdominal binding during CPR. Crit Care Med 1982;10:509-513.
28. Sanders AB, Ogle M, Ewy GA: Coronary perfusion pressure during cardiopulmonary resuscitation. A m I Emerg Med 1985;3:11-14.
35. Sharff ]A, Pantley G, Noel E: Effect of time on regional organ perfusion during two methods of cardiopulmonary resuscitation. Ann Emerg Med 1984;13:649-656.
Annals of Emergency Medicine
15:2 February 1986
Aortic and Right Atrial Pressures During Standard and Simultaneous Compression and Ventilation CPR in Human Beings Coronary perfusion pressure, as reflected by the diastolic aortic to right atrial (Ao-RA) pressure gradient, has been shown to correlate well with coronary blood flow during standard external CPR (SE-CPR) and is an important determinant of successful cardiac resuscitation. Few studies have documented such Ao-RA gradients in human beings, however. Twenty patients sustaining out-of-hospital cardiopulmonary arrests and basic cardiac life support were instrumented with thoracic aortic and right atrial catheters on arrival in the emergency department. The mean time from arrival in the ED to catheter placement was 16.5 +- 6.0 minutes. With SE-CPR, peak systolic aortic and right atrial pressures were 73.7 + 20.2 m m Hg and 69.6 + 18.3 m m Hg, respectively. End diastolic aortic and right atrial pressures were 27.9 + 7.3 m m Hg and 20.3 + 7.2 m m Hg, respectively, with an end diastolic gradient of 7.9 + 9.1 m m Hg. Three patients had systolic Ao-RA gradients of more than 25 m m Hg, which is consistent with some cardiac compression as a mechanism of flow. Five patients also had one-minute trials of simultaneous compression and ventilation CPR (SCV-CPR). Ao-RA end diastolic gradients decreased in four of the five during SCV-CPR. No patient in this study was resuscitated successfully. We conclude that ED SECPR provides little coronary perfusion for victims of prehospital carddiac arrest. Although SCV-CPR has been shown to improve carotid blood flow in human beings, it appears to have an adverse effect on the already minimal myocardial perfusion provided by SE-CPR. [Martin GB, Carden DL, Nowak RM, Lewinter JR, Johnston W, Tomlanovich MC: Aortic and right atrial pressures during standard and simultaneous compression and ventilation CPR in human beings. Ann Emerg Med February 1986;15:125-130.]
Gerard B Martin, MD Donna L Carden, MD Richard M Nowak, MD, FACEP Jody R Lewinter, MD William Johnston, MD Michael C Tomlanovich, MD, FACEP Detroit, Michigan From the Department of Emergency Medicine, Henry Ford Hospital, Detroit, Michigan. Received for publication May 28, 1985. Revisions received August 28, 1985. Accepted for publication September 26, 1985. Presented at the University Association for Emergency Medicine Annual Meeting in Kansas City, Missouri, May 1985. Address for reprints: Gerard B Martin, MD, Department of Emergency Medicine, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, Michigan 48202.
INTRODUCTION Recent investigations of CPR have helped to elucidate mechanisms of blood flow and to document the poor regional perfusion that occurs. Although evidence generated by Rudikoff, 1 Niemann, 2 and others3, 4 has provided convincing support for the "thoracic pump" mechanism of flow, the relative role of direct cardiac compression remains unresolved, s-7 Methods of CPR that exploit the thoracic pump mechanism, such as simultaneous compression and ventilation CPR (SCV-CPR) and abdominal binding, have been shown to increase carotid flow,S,9 but have had variable effects on coronary blood flow.S-ll Although adequate myocardial perfilsion is essential for successful resuscitation 12, standard external CPR (SE-CPR) provides little coronary blood flow to the fibrillating myocardium.le, u,~3,14 During CPR in the animal model, coronary blood flow has been shown to correlate with the coronary peffusion pressure, as reflected by the diastolic aortic to right atrial (Ao-RA) pressure gradient 12,13,~s and with the diastolic aortic pressure aloneA6,17 Successful resuscitation also has been related directly to these pressures.lZ, lS 21 Most of these data have been obtained from animal models. The obvious differences between these models and the person with cardiac arrest, as well as the lack of clinical studies during resuscitation, suggest that caution be used in extrapolating these data to human beings. Although it long has been known that pressure does not necessarily indicate flow during CPR 22-24, important information may be obtained from pressure monitoring during CPR, The purpose of our investigation was to 15:2 February 1986
Annals of Emergency Medicine
125/37
ATRIAL PRESSURES Martin et al
determine the feasibility of monitoring aortic (Ao) and right atrial (RA) pressures in h u m a n beings during SECPR and SCV-CPR and to attempt to apply concepts recently developed in the animal model to the h u m a n being.
METHODS Patients with out-of-hospital cardiac arrest brought to the Henry Ford Hospital emergency department were considered for inclusion in the study if a m e m b e r of the research t e a m was present. Patients with obvious significant disease of other than cardiovascular etiology and patients w i t h prol o n g e d d o w n t i m e s were excluded. Because there was only a single adv a n c e d cardiac life support (ACLS) unit in the city of Detroit, all patients received only basic cardiac life support prior to arrival in the ED. On arrival, ACLS protocol was instituted immediately, i n c l u d i n g 1-mg doses of epinephrine every five minutes and intub a t i o n . S o d i u m b i c a r b o n a t e was administered as necessary to maintain arterial pH at more than 7.2. SE-CPR was performed using a mechanical chest compressor and ventilator (Thumper% Michigan Instruments, Grand Rapids, Michigan) with sufficient force to compress the chest 2.5 to 3 inches (80 to 100 pounds of force). Ventilation pressures were set at 30 cm H20. A 7-F, 25-cm radiopaque double lumen catheter (Cook Incorporated, Bloomington, Indiana) was inserted percutaneously into the subclavian vein and advanced to the RA. The proximal port was used for drug administration and the distal port for pressure m o n i t o r i n g . P e r c u t a n e o u s placement of a 5.8-F, 90-cm radiopaque catheter (Cook Incorporated) into the thoracic aorta using a guide wire technique through the femoral artery then was attempted. The length of catheter necessary for proper placement was estimated prior to insertion. T h e c a t h e t e r s were c o n n e c t e d to Gould Statham P-50 transducers, and simultaneous pressure tracings were recorded using Hewlett-Packard 78205D amplifiers and a H e w l e t t Packard 7758 multichannel recorder. Both transducers and fluid flush systems were set up and calibrated prior to the patient's arrival in the ED. In addition to SE-CPR, five patients also had trials of SCV-CPR as described by Chandra. 2s SCV-CPR was performed using a specially modified computerized Thumper ® at a rate of 38/126
TABLE 1. Mean values for initial pressures*
Systolic Diastolic
Aortic
Right Atrial
Ao-RA
73.7 _+ 20.2
69.6 ___ 18.3
4.1 +- 13.2
27.9 +_ 7.3
20.3 _+ 7.2
7.9 +
9.1
*All values in mm Hg.
TABLE 2. Systolic pressures for three patients with systolic Ao-RA gradients
of more than 25 m m Hg*
Aortic
Right Atrial
Patient No. 1
115.2
88,2
Ao-RA 27
Body Habitus
Patient No. 2
93.5
68.0
25.5
Stocky
Patient No. 3
62.6
36.8
25.8
Thin
Thin
*All values in mm Hg.
40 cycles per minute, ventilation pressure of 100 cm H20, and 60:40 compression to relaxation ratio. In patients receiving only SE-CPR, pressures were measured for one-minute intervals every two to five minutes during the resuscitation. In the patients receiving SCV-CPR, one-minute trials of SCV-CPR were alternated with SE-CPR every two to four minutes. In accordance w i t h guidelines specified by the H u m a n Investigation C o m m i t t e e at Henry Ford Hospital, SE-CPR was reinstituted if pressures decreased during SCV-CPR. Reported pressures represent the m e a n of 20 consecutive readings. Pressures measured during chest compression were considered systolic, and those during relaxation, diastolic. Aortic and RA systolic pressures were measured at peak levels, and all diastolic pressures were recorded at end-diastole. Supine chest radiographs were taken in all patients at the conclusion of resuscitation to assess catheter position. Differences in intravascular pressures were assessed using p a i r e d . t tests with P < .05 considered significant. All m e a n pressures are noted with standard deviations. RESULTS Data were analyzed from 20 of the 23 patients originally entered in the study. Two patients were excluded because of i m p r o p e r a o r t i c c a t h e t e r placement (the extrathoracic subclavian artery in one and the abdominal Annals of Emergency Medicine
aorta in the other). The femoral artery could not be cannulated in one patient. The study included 12 w o m e n and eight m e n with a m e a n age of 61.7 + 16.0 years. No patient was resuscitated successfully. The time from collapse until arrival in the ED was not available in two cases, but averaged 18 + 8 minutes in the remaining patients. The mean time from arrival in the ED until the first pressure tracings were obtained was 16.5 +_ 6 minutes. Initial r h y t h m s included ventricular fibrillation in ll, pulseless i d i o v e n t r i c u l a r r h y t h m in six, and asystole in three. Mean values for the initial pressures from all patients are shown (Table 1). The range for diastolic Ao-RA gradients was from -14.4 to 21.4 m m Hg, including five patients with initial diastolic Ao-RA gradients of less than 0. Although mean Ao and RA systolic pressures were not significantly different (P > .05), three patients had systolic Ao-RA gradients of more than 25 m m Hg (Table 2). Two of these had a t h i n body habitus; however, n o t all t h i n p a t i e n t s s h o w e d this systolic pressure difference. R e p r e s e n t a t i v e tracings are shown (Figures 1A and 1B). The initial systolic RA pressure was 28.9 m m Hg more than Ao in one patient. This initial difference may have been secondary to massive aspiration rather than cardiac compression because subsequent systolic pressure differences after oxygenation and suctioning were minimal (Figures 2A and 15:2 February1986
A 100
100 mm Hg
mm Hg
o'
~'~%~'v
/, /;/. L L ¢ V
V~"~ ~.~vJr~
/,
jF,
s0
j
0 Ao-RA
B 100 ]
100 mm Hg
mm Hg 50
50 • '
.
j~, 'Ao ,RA /'~
lr
J
I' [Ao-RA f
tt
"/71
/
~
I
./ i
t/I
I
[
,/
~
z~
/~
'i_J
,#
II
Ao-RA
2B). Not all patients w h o aspirated had large negative Ao-RA systolic gradients. The other three patients with systolic Ao-RA gradients of more than 25 m m Hg maintained this difference on subsequent readings as long as 20 minutes later. Thirteen patients had at least two readings separated by nine minutes or more and were assessed to determine changes in diastolic Ao-RA gradients over time. The gradient increased in five patients, decreased in three, and remained essentially u n c h a n g e d (___ difference ~ 2 m m Hg) in five (P > .05). The mean change was an increase of 1 --- 9 m m Hg, with the changes ranging from a decrease of 20.3 m m Hg to an Increase of 14.3 m m Hg. The m e a n t i m e b e t w e e n readings was 17.2 +_ 7 m i n u t e s , w i t h a range of nine to 27 minutes. There did not appear to be any consistent improvem e n t in diastolic A o - R A gradients after epinephrine administration. Aortic and RA pressures for the five patients receiving SCV-CPR in addition to SE-CPR are shown (Table 3). Although the diastolic gradient decreased in four of the five patients during SCV-CPR, the mean decrease of 3.6 +_ 4.0 m m Hg was not statistically significant (P > .05). The m e a n increase in Ao systolic pressure w i t h SCV-CPR was 2.3 _+ 9.4 m m Hg and also was not statistically significant (P > .05). These data compare only the initial minute of SCV-CPR with the preceding tracing of SE-CPR. The 0nly 15:2 February 1986
patient to show an increase in diastolic Ao-RA gradient with SCV-CPR was the same patient noted earlier to have massive aspiration. This patient had an initial i m p r o v e m e n t in diastolic gradient from 11.5 m m Hg to -8.3 m m Hg with SCV-CPR. During a final trial of SE-CPR five m i n u t e s later, the gradient increased further to 0 m m Hg (Figure 2B). The other four patients underwent at least two comparisons of SCV-CPR and SE-CPR and showed a significant decrease in diastolic Ao-RA gradients of 5.1 + 2 m m Hg with SCV-CPR (P < .01). There was an increase in systolic Ao pressure of 3.0 +- 10.2 m m Hg, but this was not significant (P > .05). T h e diastolic A o - R A gradient showed a large decline over time with SCV-CPR in two patients with multiple comparisons. The gradient during SE-CPR was better sustained in these patients. For example, one patient had a decrease in diastolic Ao-RA gradient of 5.5 m m Hg over a 27-minute period with SE-CPR, compared to a drop of 16.2 m m Hg with SCV-CPR (Table 4).
DISCUSSION The rationale for using the coronary perfusion pressure (CPP), as estimated by the diastolic A o - R A gradient, as an index of coronary blood flow has b e e n e s t a b l i s h e d in t h e a n i m a l model.X2A3, Is A l t h o u g h few studies have measured this gradient In h u m a n beings, it is feasible as evidenced by our success rate of 87%. McDonald Annals of Emergency Medicine
FIGURE 1. Samples of actual tracings
obtained during CPR in two patients. A o - R A is the subtraction circuit providing continuous tracings of AoRA gradient. A. Patient showing evidence for the thoracic pump mechanism with near equality of Ao and RA systolic pressures. B. Patient showing evidence of cardiac compression with Ao-RA systolic gradients of approximately 27 m m Hg. FIGURE 2. Tracings from patient with massive aspiration. A. Initial tracings show large negative systolic and diastolic gradients. B. Tracings obtained ten minutes later show resolution of negative gradients and equality of systolic and diastolic Ao and RA pressures. has reported two six-patient series of p a r a m e d i c - t r e a t e d , refractory, prehospital cardiac arrests. In the first series, 26 diastolic gradients were less than 7 m m Hg in four cases. One patient had a gradient of 11 m m Hg, and another with a 16-mm-Hg CPP gradient was a l o n g - t e r m survivor. In McDonald's most recent series, 2z the C.PP a v e r a g e d 5.2 + 3.0 m m Hg. Sanders zs reported six p a t i e n t s in w h o m radial a r t e r y rather than Ao pressure was m o n i t o r e d along with central venous pressure, and he noted a mean diastolic gradient of 1 m m Hg. Howard 29 has monitored central venous and thoracic aortic pressures in 14 127/39
ATRIAL PRESSURES Martin et al
patients undergoing both SE-CPR and interposed abdominal compression CPR. A m e a n gradient of 2.6 m m Hg was obtained during SE-CPR. Our reported diastolic Ao-RA gradient of 7.9 + 9.1 m m Hg is higher than previously reported, b u t still is low w h e n compared to experimentally determined m i n i m u m perfusion press u r e s . D o w n e y , u s i n g an i s o l a t e d f i b r i l l a t i n g h e a r t model, has s h o w n pressure gradients of 18 m m Hg and 28 m m Hg to be necessary for subepicardial and subendocardial flow, respectively.30 These values are not dir e c t l y a p p l i c a b l e to t h e ED p a t i e n t because they were obtained in unobstructed, m a x i m a l l y dilated coronary arteries. In a study of 14 dogs undergoing CPR, N i e m a n n 19 found a diastolic A o - R A gradient of 18 m m Hg to be predictive of successful defibrillation. In another study, he found a significant difference between Ao-RA grad i e n t in survivors (23 + 6 m m Hg) and nonsurvivors {10 + 7 m m Hg). ~o R a l s t o n 12 r e p o r t e d a m i n i m u m gradient of 15 m m Hg necessary for resuscitation and short-term survival. In spite of their limitations, these pressures are of some use in setting minim u m coronary perfusion pressure requirements. A o r t i c diastolic pressure alone has been shown to correlate w i t h coronary blood flow16,17 and successful resuscitation.2O, ~1 R e d d i n g 18 s h o w e d t h a t w h e n Ao diastolic pressure could be raised to 40 m m Hg, dogs were resuscitated successfully from asphyxial arrest. Resuscitation was unsuccessful if this m i n i m u m d i a s t o l i c p r e s s u r e was not achieved. The aortic diastolic pressure of 27.9 + 7.3 m m Hg noted in our study falls below the m i n i m u m of 40 m m Hg set b y Redding, b u t above t h e 22 m m Hg n e c e s s a r y for successful defibrillation noted by N i e m a n n . 2o A l t h o u g h caution m u s t be used in extrapolating these n u m bers derived from animals to ED patients w i t h coronary artery disease, it is clear t h a t SE-CPR provides l i t t l e myocardial perfusion. T h e r e were no s u r v i v o r s in o u r study despite the fact that 11 patients p r e s e n t e d in v e n t r i c u l a r f i b r i l l a t i o n . There are three reasons for this high mortality. Most important is the prolonged downtime prior to institution of ACLS measures. C u m m i n g s 31 recently has shown that ACLS m u s t be instituted within ten to 12 m i n u t e s of collapse to be effective. Second, pa-
40/128
TABLE 3. Mean values for initial pressure readings in patients having both
SE-CPR and SCV-CPR*
Aortic Right Atrial Ao-RA Type of CPR (Systolic/Diastolic) (Systolic/Diastolic) (Systolic/Diastolic) SE-CPR
88.4 + 29.2 28.1 _+ 9.1
86.2 + 18.9 17.5 _+ 9.3
2.2 + 19.9 10.5 + 13.3
SCV-CPR
90.7 + 24.9 24.4 _+ 13.4
88.6 + 13.4 17.4 _+ 10.0
5.7 + 17.3 6.9 -+ 10.2
*All values in mm Hg,
tients who were resuscitated successfully were defibrillated soon after arrival in the ED, prior to the placement of the Ao and RA lines. Third, the gradients obtained with SE-CPR were far below e s t i m a t e d m i n i m u m coronary p e r f u s i o n p r e s s u r e r e q u i r e m e n t s . If Ao-RA gradients are valid indicators of coronary perfusion, successful resuscitation would not be expected in these patients. The lack of survivors m a y l i m i t the interpretation of this study, however. If Ao-RA gradients are not valid indicators of myocardial perfusion, survival m a y be possible w i t h low gradients. This possibility cannot be excluded w i t h the current data. As noted, five patients had initial Ao-RA gradients of less than 0, implying retrograde flow of venous blood through the coronary circulation. Such negative coronary perfusion pressures have been noted by McDonald 26 and Sanders. 28 Although the exact significance of negative perfusion pressures remains to be determined, it is probably associated w i t h perfusion of the m y o c a r d i u m w i t h deoxygenated venous blood and a nonresuscitatable heart. Initial theories on the m e c h a n i s m of flow during CPR presumed that the heart was compressed against the stern u m , l e a d i n g t o t h e e j e c t i o n of blood. 3~ More recent data have provided a convincing argument for the t h o r a c i c p u m p as a m e c h a n i s m of flow.l, a A c c o r d i n g to t h i s t h e o r y , global increases in intrathoracic pressure cause blood flow with the heart acting merely as a conduit. Equalization of systolic pressures in the RA and Ao, as seen in the majority of patients in our study, provides evidence supporting the thoracic p u m p mechanism of flow. Although other limited human data support the thoracic p u m p theory,g, 4 the three patients in
Annals of Emergency Medicine
our s t u d y w i t h s y s t o l i c A o - R A gradients of more than 25 m m Hg presumably had cardiac compression contributing to flow. In the presence of cardiac compression, one w o u l d exp e c t t h e large s y s t o l i c A o - R A gradients as seen in these patients, g3 Two of these three patients were small and thin-chested, a body habitus more l i k e l y to lend itself to cardiac compression. 6 The 15% of patients w i t h e v i d e n c e of cardiac c o m p r e s s i o n in our study compares favorably w i t h the 30% proposed by Rudikoff. 1 In Chandra's original study of SCVCPR in h u m a n beings, there was a significant increase in m e a n systolic radial artery pressure from 40.6 to 53.1 m m Hg. 2s M c D o n a l d , 27 h o w e v e r , found a decrease in systolic pressures from 112 + 7.3 to 93 + 8.1 m m Hg. O u r d a t a s h o w no s i g n i f i c a n t difference between the two techniques. The reason for the discrepancy in results is not clear. T h e small sample size a n d large v a r i a n c e in s y s t o l i c pressures are l i m i t i n g factors in our study. C o r o n a r y blood flow d u r i n g SCVCPR in the a n i m a l m o d e l has been shown to either increase minimally8,10,16 or r e m a i n t h e s a m e . n Sanders 34 was u n a b l e to r e s u s c i t a t e any dogs that received SCV-CPR w i t h a b d o m i n a l b i n d i n g , b u t five of six dogs t h a t had SE-CPR were resuscitated successfully. A significantly l o w e r A o d i a s t o l i c a n d A o - R A dia s t o l i c p r e s s u r e g r a d i e n t w e r e prop o s e d as p o s s i b l e r e a s o n s for t h e failure. Babbs, 6 however, found coron a r y p e r f u s i o n p r e s s u r e to be unchanged with SCV-CPR in a series of 12 dogs. Survival was not addressed in this study. Niemann19 found survival as well as Ao-RA gradients to be increased in animals receiving SCV-CPR with
15:2 February 1986
T A B L E 4. A o - R A diastolic gradients comparing SE-CPR w i t h SCV-CPR over time*
SE
SCV
SE
CPR Type SE SCV
SE
SCV
SE
Time after arrival in ED (min)
10
12
14
17
19
34
36
37
Ao-RA diastolic (mm Hg)
21.4
18.3
25.6
21.3
13.4
15.9
2.1
15.9
*This patient demonstrates a decrease in gradient of 5.5 mm Hg with SE-CPR, compared to a decrease of 16.2 mm Hg with SCV-CPR during the same period.
pneumatic vest and binder when comp a r e d t o SE-CPR. M c D o n a l d 2z reported a m i n i m a l increase in coronary perfusion pressure from 3 m m Hg to 3.4 m m Hg w i t h SCV-CPR in five patients. Although our readings for initial d i a s t o l i c A o - R A g r a d i e n t s were not significantly different w i t h SCVCPR, the patient w i t h aspiration mentioned previously does skew the results. W h e n f u r t h e r trials w i t h t h e other four patients were analyzed, a statistically significant decrease w i t h SCV-CPR was found. It m u s t be emphasized that although this decrease in diastolic Ao-RA gradients is numerically significant, it may not be clinically significant. SCV-CPR in our experience, however, does not improve CPP and m a y well have an adverse effect on this important index of coronary blood flow. Thus, although SCVCPR m a y lead to improved neurological recovery by virtue of its increasing cerebral blood flow, could it ultimately decrease survival by decreasing coronary blood flow? Further h u m a n studies with large numbers of patients are needed to address this question. Few studies have addressed the duration of CPR as it relates to organ flow. Sharff 3s found a significant decrease in blood flow to the heart and brain at ten m i n u t e s of CPR compared to two minutes. There was no consistent decline in diastolic Ao-RA gradients w i t h t i m e in our study. In fact, several patients showed m a r k e d improvement in their gradients. Improvement m a y have been related to catecholamine administration, correction of acidosis, adequate oxygenation, or other factors n o t y e t identified. In Some patients, the vasculature m a y be more r e s p o n s i v e to t h e r a p y d u r i n g prolonged CPR than previously t h o u g h t . In a.ddition, t h e s p e c i f i c cause of cardiac arrest was not verified by autopsy and m a y have had an effect on C P R h e m o d y n a m i c s and the 15:2February 1986
changes w i t h t i m e and therapy. Diastolic Ao-RA gradients seemed to be better maintained over time w i t h SECPR t h a n w i t h SCV-CPR (Table 4). The reason for this effect is not clean CONCLUSION Invasive monitoring of Ao and RA p r e s s u r e s in t h e ED is feasible and m a y yield clinically valuable information to guide resuscitation efforts. ED SE-CPR provides little CPP for vict i m s of out-of-hospital cardiac arrest, with clinically obtained pressures m u c h below m i n i m u m requirements derived from animal models. Although SCV-CPR m a y improve cerebral b l o o d flow, e v i d e n c e f r o m t h i s l i m i t e d s t u d y suggests t h a t it m a y have an adverse effect on the already m i n i m a l m y o c a r d i a l p e r f u s i o n provided by SE-CPR. Further studies in h u m a n beings are needed to examine diastolic Ao-RA gradients during CPR to define their prognostic importance a n d r e s p o n s i v e n e s s to t h e r a p e u t i c modalities, including "new" techniques of CPR. The authors acknowledge the tireless efforts of Ms Marty Racey in the preparation of this manuscript.
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assessment of heart chamber size and valve motion during cardiopulmonary resuscitation by two-dimensional echocardiography. A m Heart J 1981;102:368-373. 5. Babbs CF: New versus old theories of blood flow during CPR. Crit Care Med 1980;8:191-195. 6. Babbs CE Tacker WA, Paris RL, et al: CPR with simultaneous compression and ventilation at high airway pressure in four animal models. Crit Care Med 1982;10: 501-504. 7. Maier GW, Tyson GS, Olsen CO, et al: The physiology of external cardiac massage: High-impulse cardiopulmonary resuscitation. Circulation 1984;70:86-101. 8. Chandra N, Weisfeldt ML, Tsitlik J, et al: Augmentation of carotid flow during cardiopulmonary resuscitation by ventilation at high airway pressure simultaneous with chest compression. A m J Cardiol 1981;48:1053-1063. 9. Niemann JT, Rosborough JP, Ung S, et al: Hemodynamic effects of continuous abdominal binding during cardiac arrest and resuscitation. A m J Cardiol 1984;53: 269-274. 10. Luce JM, Ross BK, O'Quin RJ, et al: Regional blood flow during cardiopulmonary resuscitation in dogs using simultaneous and non simultaneous compression and ventilation. Circulation 1983;67: 258-265. 11. Koehler RC, Chandra N, Guerci AD, et ah Augmentation of cere~oral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs. Circulation 1983;67:266-275. 12. Ralston SH, Voorhees WE), Babbs CF: Intrapulmonary epinephrine during prolonged cardiopulmonary resuscitation: Improved regional blood flow and resuscitation in dogs. A n n Emerg Mect 1984; 13:79-86. 13. Ditchey RV, Winkler JV, Rhodes CA: Relative lack of coronary blood flow during dosed-chest resuscitation in dogs. Circulation 1982;66:297-302. 14. Bellamy RF, DeGuzman LR, Pedersen DC: Coronary blood flow during cardio129/41
ATRIAL PRESSURES Martin et al
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Annals of Emergency Medicine
15:2 February 1986