TY - JOUR
AU - PhD, Lawrence V. Fulton,
AB - ABSTRACT Background: Ventilation through an impedance threshold device (ITD) purportedly improves hemodynamics and survivability and is given a Class IIb recommendation by the American Heart Association/American College of Cardiology for adult cardiac arrest. No studies have investigated the effects of an ITD with vasopressin. Methods and Results: This study compared return of spontaneous circulation (ROSC), time to ROSC, hemodynamics, and pharmacokinetics with and without the use of a ResQPOD ITD. Swine were randomized to three groups: cardiopulmonary resuscitation and defibrillation alone, vasopressin with ResQPOD, and vasopressin without ResQPOD. Survival differences between the cardiopulmonary resuscitation and defibrillation group versus with and without ResQPOD groups were found (p = 0.001, FET; p = 0.021, FET, respectively) but no differences between with and without ResQPOD groups (p = 0.462). A test of Cmax between the IV and IV/ResQPOD group provided limited evidence that the IV/ResQPOD group attained higher Cmax than then IV only group (U = 11.00, p = 0.097). Median Tmax and ROSC were not statistically different between the groups (U = 11.00, p = 0.314). Conclusions: Our data suggest that there is no difference in drug kinetics or clinical outcomes in terms of survivability with or without the ResQPOD. INTRODUCTION According to the Resuscitation Outcomes Consortium, out-of-hospital cardiac arrests (OOHCAs) are estimated to affect 424,000 people in the United States annually with survival rate to hospital discharge of 10.7%.1,2 It is speculated that chest compressions alone during cardiopulmonary resuscitation (CPR) may not be adequate to provide sufficient venous blood return to the heart.3 As the chest wall recoils during CPR, a small reduction in intrathoracic pressure occurs.3 The use of the ResQPOD (Advanced Circulatory, Roseville, Minnesota), an impedance threshold device (ITD), purportedly further reduces intrathoracic pressure during CPR (e.g., increases negative intrathoracic pressure) increasing venous return to the heart,4 thereby increasing cardiac output (CO). The ResQPOD was developed to augment the management of cardiac arrest during CPR.5 According to the manufacturer, the ResQPOD prevents unnecessary air from entering the thorax during CPR.5 The device purports to act like a vacuum, causing a much higher negative intrathoracic pressure allowing more venous blood flow to the heart during CPR.5 The ITD has a Class IIb, level of evidence B recommendation from the 2010 American Heart Association CPR Guidelines.6,7 Studies investigating the use of the ResQPOD have mixed results.3,8,–10 Specifically, Cabrini et al3 conducted a meta-analysis and found that most studies suggest that the use of an ITD significantly improved return of spontaneous circulation (ROSC) and early survival with OOHCA victims who underwent CPR.8 Contrary to these results, Aufderheide et al8 compared the use of an ITD to a sham ITD during OOHCA CPR and found no significant difference in survival. More recently, Aufderheide et al9 found that the ITD used for OOHCA significantly improved survival to hospital discharge with favorable neurological function and increased survival at 1 year.10 Because the ResQPOD may increase stroke volume (SV) and CO, it is postulated that use of the device can enhance circulation of lifesaving drugs, thereby, increasing survivability. Raedler et al11 found that use of the ResQPOD increased circulating epinephrine, but clinical outcomes based on drug response were not measured. More recently, Johnson et al12 compared the ResQPOD with CPR versus no ResQPOD with CPR and measured exogenous plasma epinephrine levels in a swine model. Specifically, they compared the maximum concentration (Cmax) with the time to maximum concentration (Tmax) and found no significant difference between the two groups. However, they did not investigate the hemodynamics or ROSC and emphasized further studies need to investigate these variables. Vasopressin has demonstrated similar outcomes to epinephrine with survival to hospital discharge in patients who experienced OOHCA.13,–15 In one study, vasopressin demonstrated greater survivability to hospital admission and hospital discharge after OOHCA.16 Although vasopressin has similar outcomes to epinephrine in patients with OOHCA, its pharmacokinetics vary. To date, no studies have compared the effects of an ITD on the pharmacokinetics of vasopressin, hemodynamics, or survivability. The purposes of this study were to determine the effects of ResQPOD on the pharmacokinetics of vasopressin, hemodynamics, and ROSC. METHODS This study was an experimental, prospective, between subjects design. Twenty-one male Yorkshire-cross swine, weighing between 54.3 and 68.3 kg were used for the study. They were equally assigned via a random number generator (n = 7 per group) to 1 of 3 groups: CPR/defibrillation with vasopressin and the ResQPOD, CPR/defibrillation with vasopressin without the ResQPOD, and CPR with defibrillation alone (no vasopressin, no ResQPOD). The swine were purchased from the same vendor to avoid variability, and only castrated male swine were used to reduce any confounding that may occur from hormonal effects. These weights were selected because they represented the average weight of a U.S. Army Soldier.17 The research protocol was approved by the Institutional Animal Care and Use Committee and received care according to the Animal Welfare Act and the Guide for the Use of Laboratory Animals. The swine were observed in the facility for 3 days where they received regular medical screening and fed a standard diet during the observation period to ensure a good state of health. The subjects were nothing by mouth after midnight the night before the experiment except for water. All subjects received premedication with acepromazine (0.11–0.22 mg/kg), ketamine (15–20 mg/kg), and atropine (0.04–0.4 mg/kg) intramuscularly 30 minutes before induction of anesthesia. The swine were induced with Telazol (4–8 mg/kg) and inhaled isoflurane (4%–5%). Each pig was intubated and then placed on mechanical ventilation with a tidal volume of 8 to 10 mL/kg and a rate of 10 to 14 breaths per minute via a GE Datex-Ohmeda Aestiva anesthesia machine (Datex-Ohmeda, Madison, Wisconsin). Following intubation of the swine, the investigators reduced the isoflurane to 0.5% to 2% for maintenance until the subject was placed in a nonperfusing rhythm, at which time anesthesia was stopped. Peripheral intravenous (IV) access was established in each subject for fluid replacement and medication administration. An arterial catheter was inserted into the left carotid artery using a cut-down technique for hemodynamic monitoring specifically CO, SV, and arterial blood pressure, and another arterial catheter was placed in the femoral artery for blood sampling. The status of the swine was continuously observed using the following monitors: pulse oximetry, rectal temperature, 5-lead electrocardiogram (ECG), end-tidal carbon dioxide (EtCO2), arterial blood pressure monitor, and Vigileo hemodynamics monitor (Edwards Lifesciences, Irvine, California). The IV was maintained at a keep-vein-open rate. Periods of data collection for this study were divided into 2 phases. Phase 1 was from arrest until 20 minutes had elapsed. If a subject attained ROSC, he was monitored until the end of phase 1, then entered phase 2 to be monitored for an additional 10 minutes. Data were collected for a minimum of 20 minutes. Following subject preparation, the investigators placed the swine into cardiac arrest through electrical current stimulation of the heart. For the purposes of this study, cardiac arrest was defined as a nonperfusing arrhythmia specifically ventricular fibrillation, pulseless ventricular tachycardia, or asystole. Once cardiac arrest was confirmed, the researchers discontinued anesthesia and allowed the subject to remain in cardiac arrest for 2 minutes. The rationale for this time span was determined to be the usual time required to identify arrest, begin lifesaving measures during a witnessed cardiac arrest.9 Following 2 minutes of arrest in the swine, the researchers began administering compressions at a rate of 100 compressions per minute to a depth of 2 inches using the Michigan Life-Stat mechanical CPR device (Michigan Instruments, Grand Rapids, Michigan), which was used to provide consistent compressions that were accurate and reproducible over time and between subjects. The swine were manually ventilated at a rate of 1 breath every 6 to 8 seconds at a tidal volume of approximately 500 mL using 100% oxygen without interrupting compressions. These compression rates, depth of compressions, and ventilations were consistent with the American Heart Association 2010 Guidelines.7 For swine in the ResQPOD group, the device was placed between the endotracheal tube and the breathing circuit before the initiation of CPR in the experimental group; the control group received standard compressions and ventilation without a ResQPOD. A third group received CPR with defibrillation only. After 2 minutes of CPR, the researchers administered a one-time dose of vasopressin 40 IU intravenously followed with a normal saline bolus of 20 mL. Serial blood samples of 10 mL were collected at 0.5, 1, 1.5, 2, 2.5, 3, and 4 minutes after vasopressin injection. A 10-mL waste was drawn before each sample collection, and the arterial line was flushed to maintain patency. Once the last sample was collected, the investigators performed biphasic defibrillation of the subjects at 200 J. CPR was continued, and defibrillation at 360 J was then repeated every 2 minutes for swine that had a rhythm that necessitated defibrillation. Defibrillation before the collection of all samples was deferred because successful ROSC in some swine would have confounded the analyses of vasopressin pharmacokinetics, which was one of the primary purposes of this study. Those subjects that achieved ROSC were monitored for an additional 20 minutes following ROSC. For subjects in the ResQPOD group, the device remained in place during CPR, but was removed immediately after ROSC was achieved. The analysis of the pharmacokinetics of vasopressin was performed using high-performance liquid chromatography with tandem mass spectrometry, which is one of the most accurate spectral techniques used in the analysis of biotransformation compounds.18 RESULTS The “average” pig weighed 65.85 kg, had a base pulse rate of about 80 beats per minute, and a base temperature of 37°C. This “average” Yorkshire had a CO of 6.12 L/min, a SV of 77.62 mL, and a mean arterial pressure (MAP) of 79.67 mm Hg. O2 saturation for the “average” pig was 91.9%. Statistics for Cmax, Tmax, ROSC, and survival (a proportion) are shown in the table; however, three of these measures have fewer observations. Specifically, nine animals did not survive, so n = 12 for ROSC. Only two groups received treatment, so n = 14 for Tmax and Cmax. Next, we generated descriptive statistics for the covariates by group to investigate how well the randomization worked (Table I). In most cases, measures of center and variation were similar for the covariates, indicating that randomization appeared to be effective. We then ran Kruskal–Wallis tests (a nonparametric version of analysis of variance appropriate when parametric assumptions may not hold). Two covariates were statistically different at the α = 0.05 level: Base MAP (, p = 0.042) and Base O2 saturation (, p = 0.017). In both cases, the differences were judged to be clinically insignificant. TABLE I. Descriptive Statistics by Group, Independent Variables N = 7 for All Cells  CPR/defibrillation  IV  IV/ResQPOD  Mean  Median  Seconds  Mean  Median  Seconds  Mean  Median  Seconds  Weight in Kg  65.90  67.00  7.69  68.30  69.60  7.71  63.34  62.10  2.92  Base Pulse (Beats per Minute)  73.86  74.00  12.23  83.00  75.00  15.70  81.86  78.00  18.08  Base Temperature in °C  37.00  37.30  0.84  37.37  37.40  0.93  37.61  37.60  0.58  Base CO  6.07  5.80  1.77  7.10  6.40  1.68  5.19  5.90  1.45  Base SV  84.43  76.00  29.37  80.14  83.00  13.70  68.29  77.00  24.33  Base MAP, Hg  75.00  71.00  11.78  92.14  85.00  13.18  71.86  76.00  13.31  Base CO2  40.83  40.00  3.55  46.71  46.00  7.23  42.43  40.00  6.45  Base O2, %  84.86  90.00  14.97  93.29  93.00  4.35  97.57  96.00  2.30  N = 7 for All Cells  CPR/defibrillation  IV  IV/ResQPOD  Mean  Median  Seconds  Mean  Median  Seconds  Mean  Median  Seconds  Weight in Kg  65.90  67.00  7.69  68.30  69.60  7.71  63.34  62.10  2.92  Base Pulse (Beats per Minute)  73.86  74.00  12.23  83.00  75.00  15.70  81.86  78.00  18.08  Base Temperature in °C  37.00  37.30  0.84  37.37  37.40  0.93  37.61  37.60  0.58  Base CO  6.07  5.80  1.77  7.10  6.40  1.68  5.19  5.90  1.45  Base SV  84.43  76.00  29.37  80.14  83.00  13.70  68.29  77.00  24.33  Base MAP, Hg  75.00  71.00  11.78  92.14  85.00  13.18  71.86  76.00  13.31  Base CO2  40.83  40.00  3.55  46.71  46.00  7.23  42.43  40.00  6.45  Base O2, %  84.86  90.00  14.97  93.29  93.00  4.35  97.57  96.00  2.30  View Large TABLE I. Descriptive Statistics by Group, Independent Variables N = 7 for All Cells  CPR/defibrillation  IV  IV/ResQPOD  Mean  Median  Seconds  Mean  Median  Seconds  Mean  Median  Seconds  Weight in Kg  65.90  67.00  7.69  68.30  69.60  7.71  63.34  62.10  2.92  Base Pulse (Beats per Minute)  73.86  74.00  12.23  83.00  75.00  15.70  81.86  78.00  18.08  Base Temperature in °C  37.00  37.30  0.84  37.37  37.40  0.93  37.61  37.60  0.58  Base CO  6.07  5.80  1.77  7.10  6.40  1.68  5.19  5.90  1.45  Base SV  84.43  76.00  29.37  80.14  83.00  13.70  68.29  77.00  24.33  Base MAP, Hg  75.00  71.00  11.78  92.14  85.00  13.18  71.86  76.00  13.31  Base CO2  40.83  40.00  3.55  46.71  46.00  7.23  42.43  40.00  6.45  Base O2, %  84.86  90.00  14.97  93.29  93.00  4.35  97.57  96.00  2.30  N = 7 for All Cells  CPR/defibrillation  IV  IV/ResQPOD  Mean  Median  Seconds  Mean  Median  Seconds  Mean  Median  Seconds  Weight in Kg  65.90  67.00  7.69  68.30  69.60  7.71  63.34  62.10  2.92  Base Pulse (Beats per Minute)  73.86  74.00  12.23  83.00  75.00  15.70  81.86  78.00  18.08  Base Temperature in °C  37.00  37.30  0.84  37.37  37.40  0.93  37.61  37.60  0.58  Base CO  6.07  5.80  1.77  7.10  6.40  1.68  5.19  5.90  1.45  Base SV  84.43  76.00  29.37  80.14  83.00  13.70  68.29  77.00  24.33  Base MAP, Hg  75.00  71.00  11.78  92.14  85.00  13.18  71.86  76.00  13.31  Base CO2  40.83  40.00  3.55  46.71  46.00  7.23  42.43  40.00  6.45  Base O2, %  84.86  90.00  14.97  93.29  93.00  4.35  97.57  96.00  2.30  View Large Base MAP was statistically higher for the IV group versus the IV/ResQPOD group (Mann–Whitney U = 8.00, p = 0.038), whereas the Base O2 favored the IV/ResQPOD group over the IV group (Mann–Whitney U = 5.5, p = 0.011) and over the CPR/defibrillation group (Mann–Whitney U = 4, p = 0.007). Descriptive analysis of the primary response variables (ROSC, Survival, Cmax, and Tmax) by group illustrate that none of the CPR/defibrillation group survived thus generating no Cmax, Tmax, and ROSC values. Further, all of the IV group survived, and 5 of the 7 IV/ResQPOD group survived. Of interest, the ROSC appears to be quicker for the IV/ResQPOD while the survival proportion is lower. Table II provides the descriptive statistics for the primary response variables. TABLE II. Descriptive Statistics by Group for the Primary Response Variables    CPR/defibrillation  IV  IV/ResQPOD  Mean  Median  Seconds  Mean  Median  Seconds  Mean  Median  Seconds  Cmax/1,000 (n = 14)  N/A  N/A  N/A  70.72  55.73  28.12  103.91  101.13  35.79  Tmax in Minutes (n = 14)  N/A  N/A  N/A  1.71  1.50  0.70  2.00  1.00  1.41  ROSC Seconds (n = 12)  N/A  N/A  N/A  526.43  480.00  239.96  436.00  370.00  232.44  Survival % (n = 21)  0.00  0.00  0.00  1.00  1.00  0.00  0.71  1.00  0.49     CPR/defibrillation  IV  IV/ResQPOD  Mean  Median  Seconds  Mean  Median  Seconds  Mean  Median  Seconds  Cmax/1,000 (n = 14)  N/A  N/A  N/A  70.72  55.73  28.12  103.91  101.13  35.79  Tmax in Minutes (n = 14)  N/A  N/A  N/A  1.71  1.50  0.70  2.00  1.00  1.41  ROSC Seconds (n = 12)  N/A  N/A  N/A  526.43  480.00  239.96  436.00  370.00  232.44  Survival % (n = 21)  0.00  0.00  0.00  1.00  1.00  0.00  0.71  1.00  0.49  View Large TABLE II. Descriptive Statistics by Group for the Primary Response Variables    CPR/defibrillation  IV  IV/ResQPOD  Mean  Median  Seconds  Mean  Median  Seconds  Mean  Median  Seconds  Cmax/1,000 (n = 14)  N/A  N/A  N/A  70.72  55.73  28.12  103.91  101.13  35.79  Tmax in Minutes (n = 14)  N/A  N/A  N/A  1.71  1.50  0.70  2.00  1.00  1.41  ROSC Seconds (n = 12)  N/A  N/A  N/A  526.43  480.00  239.96  436.00  370.00  232.44  Survival % (n = 21)  0.00  0.00  0.00  1.00  1.00  0.00  0.71  1.00  0.49     CPR/defibrillation  IV  IV/ResQPOD  Mean  Median  Seconds  Mean  Median  Seconds  Mean  Median  Seconds  Cmax/1,000 (n = 14)  N/A  N/A  N/A  70.72  55.73  28.12  103.91  101.13  35.79  Tmax in Minutes (n = 14)  N/A  N/A  N/A  1.71  1.50  0.70  2.00  1.00  1.41  ROSC Seconds (n = 12)  N/A  N/A  N/A  526.43  480.00  239.96  436.00  370.00  232.44  Survival % (n = 21)  0.00  0.00  0.00  1.00  1.00  0.00  0.71  1.00  0.49  View Large A Fisher exact test (FET) indicated survival differences between the CPR and defibrillation group versus the IV-only group (p = 0.001, FET) and the IV and ResQPOD group (p = 0.021, FET), respectively. No survival differences existed between the with and without ResQPOD groups (p = 0.462, FET). The odds of survival without versus with the ResQPOD were 1.4 (0.29, 6.6), again, not statistically significant. After conducting these tests, we restricted our analysis to the IV and IV/ResQPOD groups, as the CPR and defibrillation group had no other associated dependent measures, since the animals did not recover. A Mann–Whitney test of Cmax between the IV and IV/ResQPOD group provided limited evidence that the IV/ResQPOD group attained higher Cmax than then IV only group (U = 11.00, p = 0.097). Median Tmax values were not statistically different between groups (U = 22.50, p = 0.811). Median ROSC was not statistically different between the groups (U = 11.00, p = 0.314). Figure 1 is the ROSC recovery (survival) curves, illustrating the similarity of the groups. FIGURE 1. View largeDownload slide IV versus IV/ResQPOD recovery times distribution. FIGURE 1. View largeDownload slide IV versus IV/ResQPOD recovery times distribution. As a secondary analysis, we were also interested in evaluating changes from baseline after 4 minutes of intervention for CO, SV, and MAP. Three data entry items were not recorded from the SV and MAP at time period 4. Table III shows that for both groups, median CO and SV increased from baseline at the 4 minute mark; however, MAP decreased from baseline. Mann–Whitney tests revealed no significant differences in the median changes for changes in CO, SV, and MAP (p = 0.645, p = 0.688, p = 0.945, respectively). TABLE III. Descriptive Statistics for Delta Variables    IV  IV/ResQPOD  Mean  Median  Seconds  n  Mean  Median  Seconds  n  Delta CO  1.00  1.70  2.73  7.00  1.44  1.50  2.99  7.00  Delta SV  1.84  24.00  45.97  5.00  −0.71  2.00  28.33  7.00  Delta MAP  −4.67  −38.50  70.61  6.00  −16.43  −34.00  38.64  7.00     IV  IV/ResQPOD  Mean  Median  Seconds  n  Mean  Median  Seconds  n  Delta CO  1.00  1.70  2.73  7.00  1.44  1.50  2.99  7.00  Delta SV  1.84  24.00  45.97  5.00  −0.71  2.00  28.33  7.00  Delta MAP  −4.67  −38.50  70.61  6.00  −16.43  −34.00  38.64  7.00  View Large TABLE III. Descriptive Statistics for Delta Variables    IV  IV/ResQPOD  Mean  Median  Seconds  n  Mean  Median  Seconds  n  Delta CO  1.00  1.70  2.73  7.00  1.44  1.50  2.99  7.00  Delta SV  1.84  24.00  45.97  5.00  −0.71  2.00  28.33  7.00  Delta MAP  −4.67  −38.50  70.61  6.00  −16.43  −34.00  38.64  7.00     IV  IV/ResQPOD  Mean  Median  Seconds  n  Mean  Median  Seconds  n  Delta CO  1.00  1.70  2.73  7.00  1.44  1.50  2.99  7.00  Delta SV  1.84  24.00  45.97  5.00  −0.71  2.00  28.33  7.00  Delta MAP  −4.67  −38.50  70.61  6.00  −16.43  −34.00  38.64  7.00  View Large Finally, we evaluated median concentrations of vasopressin over time between the IV and IV/ResQPOD groups. Figure 2 illustrates the median concentrations over time with imputations at 2.5 and 3.5 minutes, as data were not gathered during these times. The total number of observed points was six, and for each point, the median concentration was higher for the IV/ResQPOD group as the plot illustrates. A two-tailed binomial test (sign test) shows that the probability of obtaining six dominating points under the assumption of equal likelihood is p = 0.031. FIGURE 2. View largeDownload slide Plot of vasopressin concentrations between the 2 treatment groups. FIGURE 2. View largeDownload slide Plot of vasopressin concentrations between the 2 treatment groups. DISCUSSION The ResQPOD ITD was designed to increase SV and CO during CPR by increasing negative pressure in the thorax. This increased negative pressure purportedly enhances venous return as the chest wall recoils, thus, increasing CO and the delivery of drugs to their receptor sites. Numerous human and animal studies have shown improvement in blood flow to the heart with the use of the ResQPOD.5 Human studies showed that systolic blood pressure was greater than that of the similar control groups, and that cardiac perfusion pressures increased up to 70%.19,20 Epinephrine delivery in circulation during CPR using the ResQPOD has been shown to improve outcomes,12 but no studies had been done using vasopressin. We hypothesized that the ResQPOD increases the circulation of vasopressin during CPR, which would significantly improve cerebral and myocardial blood flow without increasing oxygen consumption. Vasopressin was shown to be a better alternative to epinephrine, which increases myocardial oxygen demand based on its adrenergic properties. Our results demonstrated that there was no significant difference between the groups that received vasopressin only (control group) and the group that received vasopressin with the ResQPOD (experimental group). The fact that 2 of the porcine models in the vasopressin with ResQPOD group did not survive, but all of the subjects in the vasopressin without the ResQPOD group survived, indicates that vasopressin without the use of the ResQPOD is optimal for the resuscitation of subjects after cardiac arrest. The effectiveness of CPR with vasopressin without the ResQPOD to achieve ROSC was significantly higher than the group with CPR and defibrillation only. Stronger evidence of the effectiveness of vasopressin was demonstrated by all of the models in the CPR with vasopressin only group achieving ROSC, but none of the models in the CPR with defibrillation alone group survived. Our research showed that the administration of 40 IU of vasopressin via the IV route during cardiac arrest resulted in a significantly higher survival (ROSC) rate than CPR with defibrillation only. This study is important not only for showing the effectiveness of delivering the optimal dose and route of administration of vasopressin to patients in cardiac arrest, it also addresses the spending of millions of dollars on a device that has not been definitively shown to be as effective as vasopressin alone. The U.S. government has spent over $17 million on the ResQPOD ITD.5 Based on the results of our study, the U.S. Army should conduct a cost–benefit analysis to determine the need to continue supplying Army hospitals with the device. Fiscal responsibility in this climate of budget constraints remains a top priority of the Department of Defense and the Department of the Army.21 In conclusion, this study showed that performing CPR with vasopressin without the use of the ResQPOD appears to be as effective as performing CPR with vasopressin with the use of the ResQPOD in increasing the chance of ROSC after cardiac arrest in a small-sample swine study. In the Advanced Cardiac Life Support algorithms, vasopressin may be used in place of the first or second dose of epinephrine.7 Further research is needed to compare the effects of intravenous vasopressin with intravenous epinephrine. If vasopressin is more effective in improving survivability, hemodynamics, and neurologic functioning than epinephrine, changing the standard to using vasopressin as the first drug in the cardiac arrest algorithm should be considered. Furthermore, if CPR using vasopressin with no ResQPOD is just as effective as CPR using vasopressin with the ResQPOD, it is all the more reason for the U.S. Government to reconsider its investment in ITDs. ACKNOWLEDGMENTS All work was performed in a Department of Defense animal laboratory located at Fort Sam Houston, Texas. This research was funded under a grant from the Tri-Service Nursing Research Program. REFERENCES 1. 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TI - Effects of the ResQPOD on Kinetics, Hemodynamics of Vasopressin, and Survivability in a Porcine Cardiac Arrest Model
JF - Military Medicine
DO - 10.7205/MILMED-D-14-00628
DA - 2015-09-01
UR - https://www.deepdyve.com/lp/oxford-university-press/effects-of-the-resqpod-on-kinetics-hemodynamics-of-vasopressin-and-yrqUKfWGwS
SP - 1011
EP - 1016
VL - 180
IS - 9
DP - DeepDyve
ER -