Interposed abdominal compression-CPR: Its effects on parameters of coronary perfusion in human subjects

ORIGINAL CONTRIBUTION CPR, and coronary perfusion; CPP,, interposed abdominal compression

Interposed Abdominal Compression-CPR: Its Effects on Parameters of Coronary Perfusion in Human Subjects

Recent literature has emphasized the relationship between coronary perfusion daring CPR and the success of resuscitation from prolonged arrest. In this study, aortic and right atrial pressures were monitored simultaneously during modifications of CPR. Three parameters associated with survival or coronary blood flow during CPR were measured: diastolic arterial pressure (DaP), diastolic arteriovenous difference (DAVD), and mean AV difference (MAVD). Standard advanced cardiac life support protocol was used although vasopressors were given by continuous infusion. In a series of two-minute trials, standard CPR, interposed abdominal compression (IAC) CPR, high- compression force (HCF) IAC-CPR, and HCF standard CPR were performed, with each patient serving as his own control. The DAP increased from 25 mm Hg during standard CPR to 43 during IAC CPR (P < .001) and 50 during HC-IAC-CPR (P < .001). The MAVD increased from 4 to 8 m m Hg during HCF-IAC-CPR (P < .05). IAC-CPR had inconsistent effects on the DAVD. Three patients had a return of spontaneous circulation during the modifications of CPR after a mean of 43 minutes of asystole with standard CPR. In the seven autopsied patients, no significant abdominal injury was found. All forms of CPR studies produced DAVD in the majority of patients well below the min imum DAVD needed for resuscitation in animal models of prolonged arrest. Although the interposed abdominal compression seems to offer some advantages over standard CPR, these hemodynamic data suggest that it would be unlikely to improve survival rates appreciably. [Howard M, Carrabba C, Foss E Janiak B, Hogan B, Guinness M: Interposed abdominal compression-CPR: Its effects on parameters of coronary perfusion in human subjects. Ann Emerg Med March 1987;16:253-259.]

INTRODUCTION Recent efforts to improve resuscitation from primary ventricular fibrilla-

tion have focused on maintaining myocardial perfusion in the arrested patient. Interposed abdominal compression CPR (IAC-CPR) is a modification of CPR with potential for improving myocardial perfusion. Hemodynamic data from three animal studies showed that IAC-CPR increases the diastolic AV pressure difference (DAVD) as compared to standard CPR by 90% to 108%. 1-3 IAC-CPR increases the diastolic arterial pressure (DAP) by 30% to 120% and the total "cardiac" output during CPR by 24% to 85%. 1,3,4 Arterial pressures monitored in six human beings during IAC-CPR showed a 50% increase in mean arterial pressure. 5 However, the only animal study directly measuring coronary blood flow found an average increase of only 5 mL/100 g/min that was statistically insignificant. 4 The clinical importance of this small increase also has been questioned.

Despite several favorable hemodynamic results, IAG has not been found to increase survival in animal studies.3, 6 A large prehospital study of IAC-CPR on patients unresponsive to initial paramedic treatment did not find any iricrease in resuscitation success in patients receiving IAC-CPR. 7

The purpose of our study was to investigate the effects of IAC-CPR on aortic (Ao) and superior vena cava (SCV) pressures in human beings. In par- ticular, the following three parameters from the CPR literature that correlate with survival or coronary blood flow were examined: mean AV pressure difference (MAVD);8,9 diastolic AV difference (DAVD);lo-17 and diastolic arterial

Mark Howard, DO Catherine Carrubba, MD Frank Foss, MD, FACS Bruce Janiak, MD, FACEP Barbara Hogan, RN, MSN Michael Guinness, MD, FACEP Toledo, Ohio

From the Departments of Emergency Medicine and the Emergency Medicine Residency of St Vincent Medical Center/ The Toledo Hospital, Toledo, Ohio.

Received for publication May 22, 1985. Revision received April 23, 1986. Accepted for publication November 14, 1986.

Presented at the University Association for Emergency Medicine Annual Meeting in Kansas City, Missouri, May 1985. Presented in part at the 1984 Scientific Assembly of the American College of Emergency Physicians in Dallas, Texas, October 1984.

Address for reprints: Michael Guinness, MD, FACEP, Emergency Medicine Residency Office, St Vincent Medical Center/The Toledo Hospital, 2213 Cherry Street, Toledo, Ohio 43608.

16:3 March 1987 Annals of Emergency Medicine 253/31

CPR & CORONARY PERFUSION Howard et al

pressure (DAP).15,17q9

MATERIALS AND METHODS Preparation and Instrumentation

In the city of Toledo, out-of-hospital cardiac arrests are managed by a two- tiered emergency medicine techni- cian/paramedic system. Standing or- ders permit endotracheal intubation, defibrillation, initiation of IV lines, and administration of the first doses of all advanced cardiac life support drugs prior to establishing radio con- tact with the base station physician.

Patients eligible for this study included both out-of-hospital cardiac arrest victims and patients who arrested in the emergency department when research personnel were available. Ex- clusion criteria included patients under 16 years of age, pregnant women, and patients with known abdominal aortic aneurysm, palpable abdominal masses, known hepatosplenomegaly, and cardiac arrest secondary to trau- ma. A specifically designated physician directed the resuscitation efforts according to American Heart Associa- tion guidelines. 2o Epinephrine was delivered by continuous infusion of 0.2 mg/min through a peripheral arm vein (equivalent to 1 mg every five minutes). After instrumentation was com- pleted, patients remaining asystolic or in pulseless idoventricular rhy thm were entered into the study. The protocol received prior approval from the appropriate committees governing human experimentation at both hospitals.

A subclavian in t roducer (Cook, Bloomington, Indiana) was placed and a multilumened catheter (Cook or Ar- row-Howe, Reading, Pennsylvania) was threaded into the superior vena cava. The femoral artery was isolated and visually identified by cutdown and a 6-F or 8-F pigtail catheter was passed into the thoracic aorta.

Two Gould-Statham (Dayton, Ohio) P23 pressure t r ansduce r s set to stretcher height were zeroed to atmo- sphere and individually calibrated. The thoracic aortic catheter and the superior vena caval catheter then were connected to the pressure transducers. The monitors used at both hospitals (Physio-Control VSM 1, Redmond, Washington; and GE A3011BC, Mil- waukee, Wisconsin) electronically in- tegrate two input channels and display the resulting mean pressures on digital displays. Graphic tracings of the si- multaneous aortic and central venous

TABLE 1. Sample size and statistical significance of each comparison made

Comparison DAP MAP DAVD MAVD

n P n P n P n P

Mechanical

St 1 vs IAC 12 < .001 14 < .01 10 < .05 14 NS*

St 1 v s S t 2 12 NS 14 NS 10 NS 14 NS

Manual

St 1 vs IAC 10 < .001 13 < .01 9 NS 13 NS

St 1 vs HC-IAC 1 0 < .001 1 3 < .01 9 NS 11 < .05

St 1 vs HC-St 10 NS 11 < .01 8 NS 11 NS

HC IAC vs HC-St 10 NS 11 NS 8 NS 11 NS

St 1 vsS t 2 6 NS. 11 NS 6 NS 11 NS

Obese vs Nonobese

HC-IAC-CPR 10 < .05 Not tested 8 NS 11 NS

*P > .05.

pressures also were recorded on a two- channel pen recorder in ten of the 14 patients studied.

Experimental Protocol Chest compressions and venti]a-

tions were performed by the Michigan Instruments (Grand Rapids, Michigan) Thumper ® during ins t rumenta t ion and Phase 1 of the protocol calling for mechanical CPR. Compression depth was set at 1.75 inches as recom- mended by the American Heart Asso- ciation. 2o For Phase 2, the Thumper ® was removed and manual CPR was done according to Association guidelines as directed by the physician in charge of resusci tat ion. Personnel doing compressions were blinded to the monitors.

Baseline arterial blood gases were drawn. Two-minute trials of different forms of CPR then were performed in the following fixed sequence: Phase l, mechanical: standard CPR (St-l), IAC- CPR (IAC), and standard CPR (St-2); Phase 2, manual: standard CPR (St-l), IAC-CPR (IAC), h igh-compress ion force (HCF)-IAC-CPR (HC-IAC), HCF standard CPR (He-St); and standard CPR (St-2). ,

Because the optimum combination of chest and abdominal compression forces is unknown, we compared different combinations. Both increases in chest compression force and the addition of IAC have individually been shown to increase pump output.l,12, ~1 HC-IAC-CPR was used to investigate

Annals of Emergency Medicine

the possibility of a synergism between these two methods.

Abdominal compression was adapt- ed from the method described by Ralston z by placing a folded, partially filled, obese blood pressure cuff longi- tudinally over the abdomen, centered at the level of the umbilicus. The ab. dominal compression began as the chest was released and was main- tained until the following chest compression began. Compressions produced peak readings of 100 to 150 mn~ Hg in the manometer attached to the abdominal cuff. During Phase 2, rescu- ers increased compression force on the chest during HC-St-CPR, and on both the abdomen and chest during HC- IAC-CPR.

At the conclusion of the study, line placement was confirmed by post- mortem chest radiograph. Age, sex, body build, evidence of clinical diffi- culties or response to the interven- tions, and time from collapse to basic life support (BLS), advanced cardiac life support (ACLS), and start of the protocol were recorded. Paramedic~ were interviewed and run sheets re. viewed for clinical signs and syrup toms preceding the arrest and for clas. sification of the arrest as witnessed o~ unwi tnessed . Autops ies were re. quested and obtained in seven pa tients.

Data Analysis Mean aortic pressure and mean cen

tral venous pressure were recorded si

32/254 16:3 March 1981

St-1 IAC St-2

Mechanical

St-1 IAC HC- HC- St-2 IAC St

Manual 1

601 50

I E 40

E ,30

20 O9 O3 10

G_ 0

St-1 IAC St-2

Mechanical


Manual 2

6 5 4 3 2 1 N v

-1 - 2

St-1 IAC St-2

Mechanical


Manual :3

9 8

z 7 E 6 g 5

4 g 3

2 (I3 4- 1

0 St-1 IAC St-2

Mechanical

multaneously from the digital display every 20 seconds, and from this the MAVD was determined.

An average DAP and DAVD were determined from the graphic pressure tracings in t en p a t i e n t s . M e a s u r e - ments were made every 0.04 seconds over three sequential CPR cycles. The CPR cycle was divided in half, and values from the second half of the cycle (CPR diastole) were averaged to give the DAP. Similarly, the DAVD was determined by averaging the AV pressure difference every 0.04 seconds during diastole of three CPR cycles.

Statistical analysis was performed by comparing each var ia t ion of CPR with the standard control trial using a paired t test. The comparisons made are shown (Table 1). P < .05 was con- sidered significant.

RESULTS Fourteen pat ients were enrol led in

the study. The mean patient age was 56 years, wi th a male:female ratio of 12:2. Two cardiac arrests were unwit- nessed; 12 were witnessed. A qualita- tive description of body bui ld found one to be th in , f ive m e d i u m , one stocky, and six obese.

For the 12 witnessed cardiac arrests,

the mean t ime from collapse to BLS was two minutes and from collapse to ACLS was 2.6 m i n u t e s . Th i s ve ry sho r t m e a n t i m e f rom co l l apse to c o m m e n c e m e n t of r e su sc i t a t i on reflects the fact that more than half of these patients were in the company of paramedics or a physician at the t ime of cardiac arrest. Mean t ime from collapse to the onset of the protocol was 45 minutes, wi th a range of 28 to 80 minutes.

Ini t ial arterial blood gas showed a mean pH of 7.22, wi th a range of 6.68 to 8.11.

The init ial rhy thm recorded by paramedics or emergency physicians was ventricular fibril lation in five patients, and bradycardia or asystole in nine.

T h r e e p a t i e n t s e n t e r e d i n to t he study had a return of spontaneous cir- c u l a t i o n i n t e r r u p t i n g the p ro toco l . The protocol was terminated early in ano the r case by the a t t end ing phy- s i c i an in order to b e t t e r m e e t the psycho log ica l needs of the pa t i en t ' s family.

Hemodynamic Effects of IAC IAC i n c r e a s e d the d i a s t o l i c and

mean arterial pressures (Table 2, Fig- ures 1 and 2).


Manual 4

F I G U R E 1. DAP during different forms of CPR.

FIGURE 2. Mean arterial pressure during different forms of CPR.

FIGURE 3. DAVD during different forms of CPR.

FIGURE 4. MAVD during different forms of CPR.

The DAP was increased especial ly by the addition of the IAC. The DAP rose from 25 m m Hg during St-CPR to 43 m m Hg and 50 m m Hg during IAC- CPR and HC-IAC-CPR, respect ively (both P < .001).

T h e e f f ec t of I A C - C P R on t h e DAVD was quite variable {Figure 3). Because both the arterial and the venous pressures increased in response to the IAC, the DAVD changed little. In the first IAC-CPR trial using mechanical IAC-CPR, the d ias to l i c AV difference decreased from 3 to - 1 m m Hg (P < .05). However, during manual IAC-CPR, the DAVD increased from 3 m m Hg to 6 m m Hg (P > .05).

The MAVD rose f rom 4 m m Hg with standard manual CPR to 8 m m Hg with HC-IAC-CPR (P < .05) (Fig-


CPR & CORONARY PERFUSION Howard et al

ure 4). The sl ight increases in the MAVD during HC-St-CPR and IAC- CPR were not significant.

Increasing Chest Compression Force

Increase in chest compression force raised the mean arterial pressure from 34 during standard manual CPR to 41 m m Hg during HC-St-CPR (P < .01) (Figure 4). A l t h o u g h slight upward t rends were observed, the MAVD, DAVD, and DAP did not increase sig- nificantly.

Body Habitus and Hemodynamic Response

The body build of 12 patients was described qualitatively at the time of the arrest. The six patients classified as obese were compared to the seven patients who were not. The obese patients had lower arterial and venous pressures during every form of CPR (Figure 5}. Dur ing HC-IAC-CPR the DAP in the obese patients was 40 m m Hg and 66 ram Hg in the nonobese (P < .05). The MAVD and DAVD did not show any consistent differences.

Clinical Response to CPR Modifications

Three of the 14 pa t ien ts in this study had a return of spontaneous cardiac activity during the protocol. A close temporal associat ion between the return of spontaneous pulse and the HC-IAC-CPR trial was noted in each case. Each of these pa t i en t s showed clear hemodynamic improvement in the minutes just prior to the return of spontaneous cardiac activity.

The first patient was a 62-year-old a lcohol ic m a n found to be febrile, tachypueic, and barely responsive to verbal stimuli prior to his cardiac arrest. After 47 minutes of asystole, a spontaneous pulse of 120 per minute and blood pressure of 134/70 m m Hg appeared. An hour later the patient arrested again and was not resuscitated. During IAC-CPR, the pressure changes noted in this patient included an increase in MAVD from 3 m m Hg to 23 m m Hg. The DAP rose from 12 m m Hg to 39 m m Hg. DAVD was not measured.

The second patient, a 62-year-old man, suffered a cardiac arrest as a compl ica t ion of biventr icular hear t failure. After 55 minutes of standard ACLS and 40 minutes of asystole, a pulse and systolic blood pressure of 90 m m Hg developed. This re turn of

TABLE 2. Mean (+ SD) of pressures during different forms of CPR

DAP MAP DAVD MAVD Mechanical

St 1 24 _+ 12 34 _+ 15 3 + 6 3 _+ 7

IAC 34 +_ 15 43 + 17 - 1 ___ 8 3 _+ 9

St 2 26 + 12 37 _+ 17 3 ___ 8 3 +_ 9

Manual

St 1 25 _+ 12 34 _+ 16 3 ___ 6 4 _+ 8

IAC 43 +_ 16 46 _+ 18 6 + 12 5 -+- 11

HC-IAC 50 _+ 23 52 _+ 17 4 _+ 19 9 + 13

HC-St 27 _+ 13 41 + 16 3 _+ 11 6 _+ 11

St 2 26 +_ 11 32 _+ 17 4 +__ 6 5 _+ 10

spontaneous c i rcula t ion lasted only eight minutes before the patient again required CPR and even tua l ly suc- cumbed. Hemodynamically the modifications of CPR had minimal effect on the MAVD and DAVD, but in this patient, the DAP rose from 34 m m Hg to 50 m m Hg during IAC-CPR, and to 53 m m Hg during HC-IAC-CPR.

The third pat ient , a 70-year-old man, had advanced coronary artery disease and chronic congestive heart failure. In the last minutes of the protocol, he developed a pulse with a systolic pressure of 40 m m Hg, deep, spontaneous respirations, and a pupil- lary response to light. The DAP in this patient increased from 38 m m Hg to 58 m m Hg during IAC-CPR. The DAVD i n c r e a s e d f r o m the c o m - paratively high control value of 16 m m Hg to 27 m m Hg during IAC-CPR and 29 m m Hg during HC-IAC-CPR. MAVD increased from the control value of 28 m m Hg to 37 rnm Hg during both IAC-CPR and HC-IAC-CPR.

Autopsy Results Seven of the fourteen patients had

autopsies. In these seven, causes of death included pulmonary saddle em- boli {one patient), acute myocardial in- farction (three), pulmonary infections (two), and cardiomyopathy with failure (one). Four patients had chronic congestion of lungs, liver, and spleen, and three had acute liver congestion with hepatomegaly. Evidence of CPR t rauma included two pat ients wi th mult iple rib fractures. One pat ient had a small laceration of the liver that was not associated with clinically significant hemoperitoneum.

DISCUSSION Significance of the MAVD

H C - I A C - C P R p roduced a statis- t ica l ly s ign i f i can t increase in the MAVD when compared to standard CPR. This is the most important dif. ference between techniques found by this study.

Of the parameters measured, the MAVD is the best of the indirect indi. cators of total sys temic blood flow. Two processes in te rac t to create MAVD in any circulatory system. The pumping of blood from the venous tG the arterial side actively generates the AV pressure difference, wh i l e pe. ripheral runoff limits the pressure dif. ference created at any given level of pump output. 22 This in teract ion is formally expressed in the following relationship: A p = CO x SVR, where A P is the mean AV difference, CO is the "cardiac" output, and SVR is the systemic vascular resistance. In dogs, Ralston 2 and Voorhees 1 have shown tha t IAC-CPR increases the total pump output . In addition, Bellamy found tha t in pigs increased chest compress ion depth increased total pump output. 12 Although total pump output was not measured directly in this study, it is most likely that the increase in MAVD reflects increased pump output f rom these modifications of CPR.

Ditchy found that the MAVD closely correlated with coronary blood flo~ measured during s tandard CPR in dogs (r = .97). 8 However, Niemanr found that the MAVD did not correlate well with resuscitation success. 23 Thus, the usefulness of this parametei has recently been questioned.

34/256 Annals of Emergency Medicine 16:3 March 1987

-T-

E

d)

70

60

50

40

30

20

10

0

St-1 IAC St-2

Mechanical


Manual 5

Diastolic AV Difference The interposed abdominal compres-

sion had l i t t le effect on the DAVD when the group is cons idered as a whole. The DAVD represents the driving pressure across the coronary circulation during the phase of the CPR cycle when t r a n s m u r a l p r e s su re is lowest, and t h i s has b e e n f o u n d to corre la te w i t h c o r o n a r y b l o o d flow.U,12,15-17 In addi t ion , N i e m a n n and Ralston have shown the DAVD to predict survival f rom pro longed arrest.15,23, 24 This study did not demon- strate significant improvement in this important parameter of coronary perfusion with IAC-CPR.

The comparative size of the arterial and venous pressure increases during the a b d o m i n a l c o m p r e s s i o n va r i ed considerably from person to person. This is reflected in the large standard deviation of the DAVD during IAC- CPR and HC-IAC-CPR (Table 1). One potential, a lbei t l imited, use of IAC- CPR is in conjunction with invasive hemodynamic monitoring. Immedia te feedback would identify the subset of patients benefiting from this maneu- ver without endangering patients wi th a negative response.

Since the complet ion of this study, Babbs has p u b l i s h e d a t h e o r e t i c a l analysis of the a b d o m i n a l compression technique suggesting methods for minimizing the diastolic venous pressure.25 T h e s e i n c l u d e f o c u s i n g a small-to-moderate compressive force along a narrow strip overlying the abdominal aorta. In contrast, the present

s tudy used more forceful abdominal compressions delivered as diffusely as p o s s i b l e over the en t i r e a b d o m e n . Confirmation that the suggested mod- if icat ions do min imize the diastol ic venous pressure is needed.

Changes in Diastolic Arterial Pressure

The la rges t and m o s t c o n s i s t e n t change seen wi th IAC-CPR is in the DAP. Because the increase in DAP was not accompanied by increases in the DAVD, the clinical importance of this finding is more difficult to evaluate.

Severa l a u t h o r s have s h o w n the DAP to correlate wi th measured coro- na ry b lood f low or to p r e d i c t survival.15,~7,18 In a classic CPR study, Redding found that dogs in asphyxial arrest resuscitated wi th methoxamine and abdominal binding wi th a DAP over 40 m m Hg could be resuscitated, whereas animals wi th a DAP below 40 could not J8 Our study found that one patient had a DAP of more than 40 during standard CPR, but seven of ten had a DAP of more than 40 m m Hg during IAC-CPR.

From the CPR li terature alone, it is not clear whether the DAP has value as an independent cor re la te of survival or whether it is more a reflection of the closely related parameter, the DAVD. However, a recent addition to the coronary perfusion l i terature and a considerat ion of a basic physiologic principle indicates that the DAP is an independent de terminant of coronary blood flow in cer tain s i tuat ions. Re-

FIGURE 5. DAP in the obese and nonobese patients during different forms of CPR.

call tha t the DAVD represen t s the "driving pressure" across the coronary circulation and the DAP the "inflow pressure."

In the l imi ted s i tua t ions in which Poiseuills ' law applies, flow through a vessel is proport ional to the driving pressure. 22 Flow will be the same for an inflow pressure (Pi) of 100 units and an outflow pressure (Po) of 0 as it is for a Pi of 200 and a Po of 100. However, in the case of dis tensible vessels or tubes, even at ident ical driving pressures (Pi - Po), flow will be greater at higher absolute levels of Pi and Po. At the h ighe r a b s o l u t e p res su res , the t r a n smura l p ressures (difference between the in t ra luminal and the extra- va scu l a r pressures) w i l l be g rea te r than at the lower pressures. The high t ransmural pressure distends the vessel d iamete r , w h i c h lowers i t s resistance.

Recently, Hanley and coworkers 27 investigated this relationship between inflow and driving pressure as deter- minan t s of flow in the coronary circulation. Using an isolated, nonwork- ing, dog h e a r t m o d e l , a c o n s t a n t driving pressure (DAVD) was created by coupling the coronary inflow and outflow pressures together. For exam- ple, to provide a driving pressure of 10 m m Hg, arterial and venous pressures, respectively, were first set at 20 and 10, and then at 50 and 40 m m Hg. Re- su l t s showed tha t w i t h a c o n s t a n t driving pressure of 10 m m Hg, no coronary blood flow occurred at inflow pressures below 20 m m Hg, but as inflow pressure was increased to 50 m m Hg, flow increased to about 50 mL/100 g/minute. The authors concluded that elevation of the intravascular pressure reduces coronary vascular resistance.

Al though the re la t ionship between inflow pressure and flow appears to be a fundamental characteristic of several vascular beds,22, 26 including the coronary c i rcu la t ion , i t s i m p o r t a n c e to human resuscitat ion has not been es- tablished. Further investigation of this relationship under the complex condi- tions of CPR is needed.

Another implicat ion of the findings of Hanley's study relevant to CPR is that the critical closing pressure is a funct ion of the t ransmura l pressure (intravascular pressure minus the ex- travascular tissue pressure) rather than

16:3.March 1987 Annals of Emergency Medicine 257/35

CPR & CORONARY PERFUSION Howard el al

the AV pressure difference per se. Ar- terial and venous pressures of 50 and 45 m m Hg, respectively, may open co ronary r e s i s t ance vessels , w h i l e pressures of 10 and 5 m m Hg may not.

Despite the finding that both the DAP and the DAVD are independent determinants of coronary blood flow, Han ley ' s obse rva t ions c o n t i n u e to support the position that the DAVD is the more important of the two. These findings are consistent with the con- cept that diastolic venous pressures should be minimized during CPR to promote coronary blood flow.

In summary, the clinical importance of the large increases in DAP unac- companied by changes in DAVD seen wi th IAC-CPR has not been estab- lished. Theoretical considerations and evidence from another model suggest that this increase may be beneficial.

Observed DAVD and the DAVD Needed for Successful Resuscitation

Several different laboratories have p r o v i d e d e s t i m a t e s of t h e DAVD needed to resusc i ta te an ima l s f rom prolonged arrest. N i e m a n n recen t ly found dogs with a DAVD of less than 17 m m Hg could not be resuscitated f rom prolonged arrest, wh i l e those over 17 m m Hg could be. 24 Ralston found that animals wi th DAVD over 25 to 30 could be resuscitated easily wh i l e those w i t h DAVD less t han about 13 to 15 m m Hg were impossi- ble to r e susc i t a t e . 15 Sanders et al found a DAVD of 30 necessary for resusci ta t ion. 17 Al though obta ined in animal models, these findings provide working est imates of the m i n i m u m DAVD needed for resusci tat ion from prolonged arrest. 28

In this study, the DAVID measured dur ing the d i f ferent forms of CPR ranged f rom 3 to 6 m m Hg. Other human studies of standard and modi- fied CPR have found similar results. M a r t i n , et a129 f o u n d an ave rage DAVD of 8 m m Hg in 22 patients during standard CPR, and 7 m m Hg in five patients during SCV-CPR. Sanders found an average DAVD of 1 m m Hg, and McDonald found that a majority of his patients had a DAVD of less than 7 m m Hg.3O, 31 It is clear that the mean DAVD found during CPR in human beings is well below the esti- mated m i n i m u m DAVD needed for delayed resuscitation. Though an oc- casional patient may reach the mini- m u m DAVD needed, 31 this is the un-

c o m m o n case. Furthermore, none of the modi f i ca t ions of CPR tes ted in human beings consis tent ly produces a DAVD t h a t equals , or even ap- proaches, these min imums.

E p i d e m i o l o g i c a l data co r robora te the impression that CPR is most often ineffective in the prolonged arrest sit- uation. Several studies indicate that the great majority of patients (84% to 86%) not resuscitated in the field by the ini t ial countershocks are not resuscitated by subsequent ACLS treatment either.32, 33

Our data support the position that a f u n d a m e n t a l l y d i f f e r en t app roach must be taken to the v ic t im of primary ventricular fibrillation who is unresponsive to initial countershocks.

C O N C L U S I O N The combination of high compres-

sion force and interposed abdominal compression increased the MAVD by a smal l but s ta t i s t ica l ly s ignif icant amoun t . IAC-CPR s ign i f i can t ly increased the diastolic arterial pressure, but had unpredictable effects on the DAVD. Fur ther deve lopmen t of the IAC technique to min imize diastolic venous pressure seems necessary prior to its empiric use.

In the m a j o r i t y of pa t i en t s , the DAVD during all the forms of CPR studied remained well below the min- i m u m needed for resusci tat ion from prolonged arrest.

The authors thank the following indi- viduals for their generous donations of time, expertise, and equipment: Charles Babbs, MD, PhD, for his thoughtful cri- tique and support; Clare Barkelow, Michi- gan Instruments, for donation of the Thumper% Martha Kreimer-Birnbaum, PhD; Marilyn Gagne, Hemodynamics Laboratory; Judy J Wenig, PhD, statisti- cian; coroner, Lucas County, Ohio; Respi- ratory Therapy Department, The Toledo Hospital; paramedic personnel of the City of Toledo; Cook Critical Care Products (Bloomington, Indiana), for donation of catheters; Stryker Corporation, Kala- mazoo, Michigan; the Biomedical, Radi- ology, and Pathology departments of both hospitals; and the nurses, physicians, clerical staff, and chaplains of both hospitals.

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2. Ralston SH, Babbs CE Niebauer MJ: Cardio-

pulmonary resuscitation with interposed ab dominal compression in dogs. Anesth And 1983;6h645-5I.

3. Hayes OW, Omans J, White BC, et ah Pr0 longed cardiac arrest and resuscitation in dogs Cardiac resuscitability and perfusion pressure: with CPR versus interposed abdominal coon pression CPR. Ann Emerg Med (in press).

4. Voorhees WD, Ralston SH, Babbs CF: Re gional blood flow during cardiopulmonary re suscitation with abdominal counterpulsation dogs. Am J Emerg Med 1984;2:123-128.

5. Berryman R, Phillips GM: Interposed abdorn inal compression-CPR in human subjects. A~ir Emerg Med 1984;13:226-229.

6. Kern KB, Carter AB, Showen L: Resuscita tion and twenty-four hour survival among thr~ different modes of manual cardiopulmonary re suscitation. Clin Research 1985;2:10A.

7. Mateer JR, Stueven HA, Thompson BM, e ah Prehospital IAC CPR versus standard CPR Paramedic resuscitation of cardiac arrest. Arn Emerg Med 1985;3:143-146.

8. Ditchey RV, Winkler JV, Rhodes CA: Relativ, lack of coronary blood flow during closed ches' resuscitation in dogs. Circulation I982;66 297-302.

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Documents

Interposed abdominal compression-CPR: Its effects on parameters of coronary perfusion in human subjects