(Circulation. 2000;101:989.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Anesthesiology and Critical Care (P.P., D.P.), Lariboisière University Hospital, Paris, France; and the Cardiac Arrhythmia Center, Cardiovascular Division (K.G.L.), University of Minnesota, Minneapolis.
| Abstract |
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Methods and ResultsThis prospective, randomized, blinded trial was performed in prehospital mobile intensive care units in Paris, France. Patients in nontraumatic cardiac arrest received ACD CPR plus the ITV or ACD CPR alone for 30 minutes during advanced cardiac life support. End tidal CO2 (ETCO2), diastolic blood pressure (DAP) and coronary perfusion pressure, and time to return of spontaneous circulation (ROSC) were measured. Groups were similar with respect to age, gender, and initial rhythm. Mean maximal ETCO2, coronary perfusion pressure, and DAP values, respectively (in mm Hg), were 13.1±0.9, 25.0±1.4, and 36.5±1.5 with ACD CPR alone versus 19.1±1.0, 43.3±1.6, and 56.4±1.7 with ACD plus valve (P<0.001 between groups). ROSC was observed in 2 of 10 patients with ACD CPR alone after 26.5±0.7 minutes versus 4 of 11 patients with ACD CPR plus ITV after 19.8±2.8 minutes (P<0.05 for time from intubation to ROSC).
ConclusionsUse of an inspiratory resistance valve in patients in cardiac arrest receiving ACD CPR increases the efficiency of CPR, leading to diastolic arterial pressures of >50 mm Hg. The long-term benefits of this new CPR technology are under investigation.
Key Words: cardiopulmonary resuscitation heart arrest circulation active compression-decompression
| Introduction |
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| Methods |
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The MICU staff included 5 persons. A MICU physician (anesthesiologist or general practitioner specially trained in emergency medicine), a nurse anesthetist, a medical student, and an ambulance driver managed the patient and helped for the performance of the protocol. In addition, there was another physician (anesthesiologist) at the scene to coordinate the research protocol. According to standard guidelines governing the French EMS system, patients with known terminal illness or in whom the delay between cardiac arrest and basic CPR exceeded 30 minutes did not receive advanced life support (ALS) CPR. Patients younger than 18 years old and those with hypothermia or thoracic trauma were also excluded from the study. The BLS and ALS teams worked together under the supervision of the EMT chief and the MICU physician. The ALS team also performed ACD CPR.
Evaluation of the rhythm was made by the MICU staff. For patients in ventricular fibrillation, European Resuscitation Council as well as American Heart Association guidelines were followed.13 14 For patients in asystole and pulseless electrical activity, ACD CPR was performed continuously by the MICU staff for a minimum of 30 minutes, unless return of spontaneous circulation was achieved. No attempt was routinely made to try to pace patients who were in asystole during the resuscitation effort. Epinephrine (1 mg) was administered every 5 minutes throughout the resuscitation effort.
All patients were intubated with an endotracheal tube on arrival of the
MICU team. Following intubation, patients were mechanically ventilated
with a compressible ventilator bag (Ambu Spur, Ambu Inc) with 100%
oxygen. Ventilation was provided with 10 L/min oxygen, at a rate of 15
breaths/min with a tidal volume of
10 mL/kg of patients weight.
Monitoring of tidal volume was made by a spirometer of Wright fixed
just before the inspiratory part of the ventilation bag valve. The
impedance valve (ITV Resusci-Valve, provided by
CPRxLLC, Minneapolis, Minn) was placed between
the endotracheal tube (just distal to the antibacterial filter) and the
connection port of the ventilator bag (Figure 1
). This valve comprises a highly
compliant silicone diaphragm, a fenestrated mount, and a safety
"pop-off" valve attached to the side of the device and set to open
when the intra-thoracic pressure decreases below -22 cm
H20. The principle of the valve is to completely
occlude the endotracheal tube when the pressure within the thorax is
below atmospheric pressure. As such, the valve prevents inspiratory gas
exchange only during the decompression phase, except during the time
that active ventilation is being performed by the rescuer. In practice,
when the patient is actively ventilated with the ventilator bag, oxygen
is passed through the fenestrated mount of the valve during
insufflation directly into the endotracheal tube without any
significant impedance. When active ventilation is not performed, the
silicone diaphragm occludes the airway whenever the intrathoracic
pressure is <0 cm of water, ie, during the active decompression phase.
During exhalation and during the compression phase of CPR, respiratory
gases pass in the reverse direction, pushing the silicone diaphragm out
of the way without any resistance by the valve.
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Using a computer-generated randomization chart, some of the valves were either enabled with the silicone diaphragm (ACD + ITV group) or disabled and the diaphragm was removed (ACD alone group). During the protocol study, it was not possible for the MICU staff to determine by visual inspection whether or not the silicone diaphragm was in place or had been removed. As such, they were blinded to use of the investigational device. When the diaphragm is removed, the valve does not impede inspiration, as there is a completely open conduit between the ventilator bag and the endotracheal tube. As such, gas exchange is not impaired and inhalation and exhalation are performed without any significant resistance. The randomization assignment was made before the beginning of the protocol by the hospital sterilization service. During performance of CPR and throughout the subsequent hospitalization, investigators were blinded to whether the impedance valve did or did not contain a functional diaphragm. After each use by the MICU staff, the valve was brought to this service for cleaning, and the sterile valve was then returned to the study physician in a bag with or without the diaphragm according to the randomization list.
Once patients were intubated by the MICU physician, a peripheral intravenous line was placed for drug administration. Femoral arterial (Seldicath, 5F, 12 cm, Plastimed, France) and venous cannula were placed sequentially by the study physician. A central venous cannula (2F, 60 cm, Seldiflex, Plastimed, France) introducer sheath was advanced 60 cm in the cranial direction in order to position the distal tip into the thoracic portion of the inferior vena cava. Arterial and central venous pressures were continuously monitored with heparinized fluid-flushed tubing to transducers (Sorensen Transpac III, Abbott Systems) and a monitoring system (Propac Encore, Physiocontrol). Transducers were calibrated and fixed to the midaxillary line of the patient. End tidal CO2 (ETCO2) was monitored continuously after intubating the patients with a capnometer (Normocap, Datex). Data from each patient were collected and analyzed to determine the ETCO2 and the arterial and right atrial pressures. The coronary perfusion pressure was calculated as the mathematical difference between arterial and right atrial pressures at the end of the relaxation phase of CPR.9 15 Hemodynamic parameters were monitored simultaneously at both catheters sites, and measurements were made every 5 minutes, just before a new epinephrine injection. If return of spontaneous circulation was achieved, CPR was discontinued and the impedance valve was removed. Patients were then ventilated with a portable volumetric ventilator (AXR1, Airox, France) and transported to the nearest inpatient hospital intensive care unit facility. All data regarding the resuscitation effort as well as postresuscitation clinical care were collected according to the Utstein Conference guidelines.10 Return of spontaneous circulation was defined as the presence of a palpable pulse in the absence of active chest compressions. Neurological outcome was evaluated using the cerebral performance category score system.10 Autopsies were not performed on the deceased.
All values are expressed as mean±SEM. Statistical analysis was performed for comparisons between groups using an unpaired 2-tailed Students t test. Statistical significance was considered to be at P<0.05. The 95% CI was also calculated for the mean difference between groups.
| Results |
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20
minutes after cardiac arrest. Five patients in asystole and 4 patients
in ventricular fibrillation were also excluded because
simultaneous femoral arterial and venous access
could not be obtained within 10 minutes (6 in the ACD alone group, 3 in
the ACD plus valve group). Twenty-one patients were prospectively
enrolled in this study. Ten patients were randomized to the ACD CPR
group and 11 were randomized to receive ACD CPR plus valve. As shown in
Table 1
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As shown in Figure 2
, ETCO2 levels were similar at the time of
intubation (t=0), but rose more rapidly and to higher peak values in
the ACD plus valve group compared with ACD CPR alone. These data
include all ETCO2 measurements while patients
were receiving CPR. In the ACD alone group, mean
ETCO2 (mean±SEM) levels increased from 6.6±2.3
to 13±0.9 mm Hg during CPR, whereas in the ACD plus valve group,
ETCO2 increased from 6.9±0.5 to 19.1±0.9
mm Hg (P<0.001 comparing maximum values). The 95% CIs for
comparison of baseline ETCO2 values between groups were
1.6, 2.2 and 2.2, 9.2 for maximal values during CPR. There were fewer
data points in the later time periods because some patients were
resuscitated. As shown in the insert of Figure 2
, in individual
patients that were resuscitated, ETCO2 increased
to >20 mm Hg, at which point asystole converted spontaneously to
a stable blood perfusing rhythm. In these patients, sinus rhythm was
restored and no additional CPR was required. This process occurred more
rapidly in the impedance valve group. No patient with an
ETCO2 <20 mm Hg was resuscitated during
the 30-minute period of ACD CPR after intubation.
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At the time the invasive monitoring was initiated (t=10 minutes),
there were marked differences between groups when comparing the
arterial pressures (Figure 3
). There was no evidence for a
compression phase gradient between the arterial and right
atrial pressures. The mean peak arterial pressures, which
were observed 10 minutes after intubation in both groups, were
90±6.4 mm Hg in the ACD CPR alone group versus 108±3.1 in the
valve group (P<0.05). The maximal mean
diastolic arterial pressure in the ACD CPR plus
valve group was 56.4±1.7 mm Hg versus 36.5±1.5 mm Hg in
the ACD alone group (P<0.001; 95% CI, 14.3, 23.8).
Patients who had ROSC (Figure 3
insert) had higher
diastolic arterial pressures in the ACD CPR
plus valve group compared with ACD CPR alone. A comparison between the
coronary perfusion pressures in patients treated with ACD plus
valve CPR versus ACD CPR alone is shown in Figure 4
. The maximal diastolic
coronary perfusion pressure with ACD CPR plus valve was
43±1.6 mm Hg versus 25.3±1.8 mm Hg for ACD CPR alone
(P<0.001; 95% CI, 12.4, 22.8). The mean coronary
perfusion pressure was 70% higher in the ACD CPR plus valve group when
compared with the group given ACD CPR alone. With ACD CPR plus valve,
patients with a coronary perfusion pressure >40 mm Hg
appeared to have a greater likelihood of ROSC.
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In the present study, the first recorded rhythm for all the
patients was asystole. Results related to time from intubation to ROSC,
survival to 24 hour, survival after day 30, and survival to hospital
discharge without neurological impairment are also shown in Table 2
for both groups of patients. There was
a significant reduction in the time between intubation and ROSC in the
valve group (n=4; t=19.8±2.8 minutes) versus ACD alone group (n=2;
t=26.5±0.7 minutes) (P=0.03).
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| Discussion |
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ETCO2 has previously been used as a surrogate for cardiac output and blood flow through the lungs, although it is affected both by blood flow and by minute ventilation.17 The measurement of ETCO2 as a surrogate for survival depends on several parameters, especially on minute ventilation. It has been previously shown that ACD CPR increased minute ventilation even during mechanical ventilation as compared with standard CPR.18 19 As such, measures of ETCO2 may be underestimated with ACD CPR.20 In contrast, because the impedance valve impedes gas exchange except during active manual ventilation, measured ETCO2 during ACD CPR plus the valve may be overestimated. Nonetheless, in the present study the higher ETCO2 values observed in the valve group were associated with a significant improvement in hemodynamic variables, such as systolic and diastolic arterial and coronary perfusion pressures and a shorter time between intubation and ROSC.
Information related to the initial cardiac rhythm in Paris is not known until the arrival of the ALS team, about 13 minutes after initiation of BLS CPR. In the present study the first recorded rhythm was asystole in all patients. This rhythm is generally associated with the worst outcome.7 21 22 However, recent studies from Paris, France, where >80% of patients were in asystole, have demonstrated that ACD CPR results in a significant improvement in a number of clinical outcomes, including hospital discharge rates (5.5%)7 21 and 1-year survival rates (4.6%)21 when compared with standard CPR (1.9%7 and 1.9%,21 respectively). As such, the hemodynamic improvement achieved by optimizing the bellows-like action of the chest with ACD CPR plus the impedance valve, as observed in the present study, suggest that patients in asystole may have an even greater chance for survival than previously considered.2
One of the limitations of the present study was that ACD CPR plus the valve could not be evaluated in patients with ventricular fibrillation, as we could not insert intravenous and arterial femoral lines in <10 minutes due to the multiple defibrillation attempts. Thus, although a benefit of the valve has previously been observed in animals,9 its potential value for patients in ventricular fibrillation remains unknown. A second limitation is that arterial blood gases were not measured in the present study. We have previously observed in the animal model that the partial pressure of arterial oxygen, PaO2, was decreased in the ACD CPR plus valve group relative to ACD CPR alone, although PaO2 values remained >95 mm Hg during CPR.9 Given the potential for decreased oxygenation despite active ventilation, PaO2 will have to be evaluated in the future. Another limitation is that femoral arterial pressures were used to calculate the coronary perfusion pressures instead of central aortic monitoring. We used a femoral arterial catheter because it is the standard of clinical practice in intensive care units. However, femoral arterial pressure measurements in cardiac arrest have been previously reported to be comparable with aortic pressures during both compression and relaxation phases of CPR in humans.23 Finally, due to previous lack of benefit associated with pacing patients in asystole in Paris, no efforts were made to externally pace the patients. Given the elevated diastolic arterial pressures and coronary perfusion pressures achieved with ACD CPR plus valve, pacing will be tried in future studies.
It is too early to know whether use of the impedance valve will improve the chances for long-term survival. This study was designed to evaluate acute hemodynamic parameters in patients with recent cardiac arrest in a well-controlled clinical environment. Larger prehospital studies are therefore needed to evaluate the likelihood of improved long-term survival with neurological recovery with this new technique. Nonetheless, this study demonstrates that use of an inspiratory impedance valve during CPR further optimizes mechanical measures associated with ACD CPR by increasing venous return and coronary perfusion pressures. Diastolic arterial pressures and coronary perfusion pressures recorded in this study with an impedance valve are >70% higher than those achieved with ACD CPR alone. These findings further underscore the importance of lowering intrathoracic pressure during the decompression phase of CPR. On the basis of these promising findings, prospective randomized clinical trials are underway to determine potential long-term value of combining ACD CPR with an impedance threshold valve in patients with cardiac arrest.
| Acknowledgments |
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| Footnotes |
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Dr Lurie is a co-inventor of the CardioPump, the device used to perform ACD CPR. Although the rights of the device are owned by the University of San Francisco, Dr Lurie was an employee of the University of California when the device was developed and is entitled to potential royalties from the sale of the device according to the rules and regulations of the Regents of the University of California. In addition, Dr Lurie is a co-inventor of the impedance threshold valve and has founded a company (CPRX) to develop the valve because the University of Minnesota Office of Research and Technology Administration was not interested in patenting the device.
Received April 30, 1999; revision received September 1, 1999; accepted September 17, 1999.
| References |
|---|
|
|
|---|
2.
Lurie KG, Shultz JJ, Callaham ML, Schwab TM, Gisch T,
Rector T, Frascone RJ, Long L. Evaluation of active
compression-decompression CPR in victims of out-of-hospital cardiac
arrest. JAMA. 1994;271:14051411.
3.
Chang MW, Coffeen P, Lurie KG, Voss G, Detloff B,
Homans DC, White CW. Active compression-decompression CPR improves
vital organ perfusion in a dog model of ventricular
fibrillation. Chest. 1994;106:12501259.
4. Lurie KG. Active compression-decompression CPR: a progress report. Resuscitation. 1994;28:115122.[Medline] [Order article via Infotrieve]
5.
Guly UM, Robertson CE. Active decompression improves
the hemodynamic state during cardiopulmonary
resuscitation. Br Heart J. 1995;73:372376.
6. Pell ACH, Pringle SD, Guly UM, Steedamn DJ, Robertson CE. Assessment of the active compression-decompression device (ACD) in cardiopulmonary resuscitation using transesophageal echocardiography. Resuscitation. 1994;27:137140.[Medline] [Order article via Infotrieve]
7.
Plaisance P, Adnet F, Vicaut E, Hennequin B, Magne P,
Prudhomme C, Lambert Y, Cantineau JP, Leopold C, Ferracci C, Gizzi M,
Payen D. Benefit of active compression-decompression
cardiopulmonary resuscitation as a prehospital advanced cardiac
life support: a randomized multicenter study. Circulation. 1997;95:955961.
8.
Lurie KG, Mulligan K, McKnite S, Deltoid B, Lindner K.
Optimizing standard cardiopulmonary resuscitation with an
inspiratory threshold valve. Chest. 1998;113:10841090.
9.
Lurie KG, Coffeen PR, Shultz JJ, McKnite SH, Deltoid
BS. Improving active compression-decompression cardiopulmonary
resuscitation with an inspiratory impedance valve.
Circulation. 1995;91:16291632.
10. Cummins RO, Chamberlain DA, Abramson NS, Allen M, Baskett P, Becker L, Bossaert L, Delooz H, Dick W, Eisenberg M. Recommended guidelines for uniform reporting of data from out-of-hospital cardiac arrest: the Utstein Style. Ann Emerg Med. 1991;20:861874.[Medline] [Order article via Infotrieve]
11. Wik L, Mauer D, Robertson C. The first European pre-hospital active compression-decompression (ACD) cardiopulmonary resuscitation workshop: a report and a review of ACD-CPR. Resuscitation. 1995;30:191202.[Medline] [Order article via Infotrieve]
12. Schneider T, Wik L, Baubin M, Dirks B, Ellinger K, Gisch T, Haghfelt T, Plaisance P, Vandemheen K. Active compression-decompression cardiopulmonary resuscitation: instructor and student manual for teaching and training, part I: the workshop. Resuscitation. 1996;32:203206.[Medline] [Order article via Infotrieve]
13.
Emergency Cardiac Care Committee and Subcommittees,
American Heart Association. Guidelines for cardiopulmonary
resuscitation and emergency cardiac care. JAMA. 1992;268:21842234.
14. ALS working party of the European Resuscitation Council. Guidelines for advanced life support. Resuscitation. 1992;24:111121.[Medline] [Order article via Infotrieve]
15.
Paradis NA, Martin GB, Goetting MG.
Simultaneous aortic, jugular bulb, and right atrial
pressures during cardiopulmonary resuscitation in humans.
Circulation. 1989;80:361368.
16. Shultz JJ, Coffeen P, Sweeney M, Detloff B, Kohler C, Pineda E, Yakshe P, Adler SW, Chang M, Lurie KG. Evaluation of standard and active compression-decompression CPR in an acute human model of ventricular fibrillation. Circulation. 89:684693.
17.
Gudipati CV, Weil MH, Bisera J, Deshmukh HG, Rackow EC.
Expired carbon dioxide: a noninvasive monitor of
cardiopulmonary resuscitation. Circulation. 1988;77:234239.
18. Tucker KJ, Khan JH, Savitt MA. Active compression-decompression resuscitation: effects on pulmonary ventilation. Resuscitation. 1993;26:125131.[Medline] [Order article via Infotrieve]
19. Carli PA, De La Coussaye JE, Riou B, Sassine A, Eledjam JJ. Ventilatory effects of active compression-decompression in dogs. Ann Emerg Med. 1994;24:890894.[Medline] [Order article via Infotrieve]
20. Orliaguet GA, Carli PA, Rozenberg A, Jannière D, Sauval P, Delpech PH. End-tidal carbon dioxide during out-of-hospital cardiac arrest resuscitation: comparison of active compression-decompression and standard CPR. Ann Emerg Med. 1995;25:4851.[Medline] [Order article via Infotrieve]
21. Plaisance P, Lurie KG, Vicaut E, Adnet F, Petit JL, Epain D, Ecollan P, Gruat R, Cavagna P, Biens J, Payen D, and the French ACD study group. A comparison of standard cardiopulmonary resuscitation versus active compression-decompression resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 1999;341:59975.
22.
Gueugniaud P, Mols P, Goldstein P, Pham E, Dubien P-Y,
Deweerdt C, Vergnion M, Petit P, Carli P. A comparison of repeated high
doses and repeated standard doses of epinephrine for cardiac
arrest outside the hospital. N Engl J Med. 1998;339:15951601.
23. Rivers EP, Lozon J, Enriquez E, Havstad SV, Martin GB, Lewandowski CA, Goetting MG, Rosenberg JA, Paradis NA, Nowak RM. Simultaneous radial, femoral, and aortic arterial pressures during human cardiopulmonary resuscitation. Crit Care Med. 1993;21:878883.[Medline] [Order article via Infotrieve]
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