Anderson 2018

Journal of Trauma and Acute Care Surgery, Publish Ahead of Print
10.1097/TA.0000000000001901
Left Ventricular Compressions Improve Return of Spontaneous Circulation
and Hemodynamics in a Swine Model of Traumatic Cardiopulmonary Arrest
Kenton L. Anderson, MD
Stanford University School of Medicine
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Department of Emergency Medicine
900 Welch Road, Ste 350
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Palo Alto, CA 94304
Kristin C. Fiala, MD
Madigan Army Medical Center

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9040 Jackson Ave
Tacoma, WA 98431
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Maria G. Castaneda, MS
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CREST Research Program
Wilford Hall Ambulatory Surgical Center

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2200 Bergquist Dr.
Lackland AFB, TX 78236
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

Susan M. Boudreau, RN, BSN
CREST Research Program
Wilford Hall Ambulatory Surgical Center
2200 Bergquist Dr.
Lackland AFB, TX 78236
Allyson A. Araña, PhD
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US Air Force En Route Care Research Center 59th MDW/ST Chief Scientist's Office
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United States Army Institute of Surgical Research
3551 Roger Brooke Drive
Fort Sam Houston, TX 78234

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Vikhyat S. Bebarta, MD
University of Colorado School of Medicine

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12401 East 17th Avenue, Campus Box L10, Rm 751
Aurora, CO 80045
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CONFLICT OF INTEREST STATEMENT:
None of the authors have any conflicts of interest to disclose.

MEETINGS:
The data contained in this manuscript were presented as a poster at the 2014 American Heart
Association Scientific Sessions, November 15-19, 2014 in Chicago, Illinois, and as an oral
presentation at the 2014 Military Health System Research Symposium, August 18-21, 2014 in
Fort Lauderdale, Florida.
FUNDING:
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This study was funded by a grant from the Office of the Air Force Surgeon General. The views
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expressed in this manuscript are those of the authors and do not reflect official policy or position
of the United States Government, Department of Defense, or the United States Air Force.
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ABSTRACT
Background: Prehospital cardiopulmonary resuscitation, including closed chest compressions,
has commonly been considered ineffective in traumatic cardiopulmonary arrest (TCPA) because
traditional chest compressions do not produce substantial cardiac output. However, recent
evidence suggests that chest compressions located over the left ventricle produce greater
hemodynamics when compared to traditional compressions. We hypothesized that chest
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compressions located directly over the left ventricle would improve return of spontaneous
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circulation (ROSC) and hemodynamics, when compared to traditional chest compressions, in a
swine model of traumatic cardiopulmonary arrest (TCPA).
Methods: Transthoracic echocardiography was used to mark the location of the aortic root
(traditional compressions), and the center of the left ventricle (LV) on animals (n=26) which
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were randomized to receive chest compressions in one of the two locations. After hemorrhage,
ventricular fibrillation (VF) was induced. After ten minutes of VF, basic life support (BLS) with
mechanical CPR was initiated and performed for ten minutes followed by advanced life support
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(ALS) for an additional ten minutes. During BLS the area of maximal compression was verified
using transesophageal echocardiography. Hemodynamic variables were averaged over the final
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two minutes of BLS and ALS periods.
Results: Five of the left ventricle group (38%) achieved ROSC compared to zero of the aortic
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root group (p=0.04). Additionally, there was an increase in aortic systolic blood pressure (SBP),
aortic diastolic blood pressure (DBP) and coronary perfusion pressure (CPP) at the end of both
the BLS (95% CI SBP -49 to -21, DBP -14 to -5.6 and CPP -15 to -7.4) and ALS (95% CI SBP -
66 to -21, DBP -49 to -6.8 and CPP -51 to -7.5) resuscitation periods among the LV group.

Conclusions: In our swine model of TCPA, chest compressions performed directly over the left
ventricle improved ROSC and hemodynamics when compared to traditional chest compressions.
Level of Evidence: Therapeutic Animal Model, Level I
Keywords: Cardiopulmonary resuscitation; Trauma; Hemodynamics; Survival;
Echocardiography
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BACKGROUND
Resuscitation of traumatic cardiopulmonary arrest (TCPA) patients in the pre-hospital
setting remains controversial. Survival rates between 0% - 3.7% have been reported among
TCPA victims, thus resuscitation of all TCPA patients has been considered by many to be futile
and an inappropriate utilization of resources (1-4). In 2003 the National Association of
Emergency Medical Services Physicians and the American College of Surgeons Committee on
Trauma established guidelines regarding the withholding or termination of out-of-hospital
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resuscitation in TCPA (5). While trauma represents the greatest threat to life for all people
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between the ages of 1-44, and the leading cause of cardiac arrest among in combat settings, the
incidence of successful cardiopulmonary resuscitation (CPR) in trauma victims at the time the
guidelines were released was largely unreported (6-9). More recent reports have described
improved survival rates with good neurologic outcomes even when CPR has been performed in a
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breach of the published guidelines (5, 10-12).
Cardiopulmonary resuscitation, including closed chest compressions, has commonly been
considered ineffective in TCPA because the cardiac output generated by closed chest
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compressions is only about 25% that of open chest compressions and may potentially cause more
trauma in a patient that is already suffering from traumatic injuries (13, 14). Fortunately, there
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have been recent advancements which may allow non-compressible hemorrhage to be controlled
by prehospital personnel, and recent laboratory research has demonstrated that chest
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compressions performed directly over the heart rather than the middle of the chest (which is
usually cephalad to the heart) improve hemodynamics and short-term survival of medical cardiac
arrest (15, 16). It is possible that the same chest compression techniques may also improve
hemodynamics and survival when applied to TCPA.

We hypothesized that chest compressions located directly over the left ventricle (LV)
would increase return of spontaneous circulation (ROSC) when compared to traditional
compressions in a swine model of TCPA. Secondary analyses included an evaluation of
hemodynamic and laboratory variables as well as short-term survival to 60 minutes between the
two groups.
METHODS
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Study Design and Setting
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We conducted a prospective, randomized comparative investigation approved by our
Institutional Animal Care and Use Committee. All procedures involving animals complied with
the regulations and guidelines of the Animal Welfare Act, the National Institutes of Health Guide
for the Care and Use of Laboratory Animals, and the American Association for Accreditation of
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Laboratory Animal Care. The housing of animals and the performance of the study took place in
the Animal Care Facility at our institution. Reporting adheres to the Animals in Research
Reporting In Vivo Experiments (ARRIVE) guidelines. (19)

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Animal Preparation
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Twenty-six female Yorkshire swine weighing 25-32kg were obtained 2-4 days before
experimentation to allow acclimation to the facility. Per the vendor, the animals were free from
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viral, bacterial and parasitic pathogens.
Animals were housed individually in 4x4 foot cages with rubberized textured flooring in
a temperature and humidity controlled building with a 12-hour light/dark cycle set on a timer.
Animals were allowed free access to water and were provided a maintenance diet (PMI Nutrition
International, LLC, Brentweed, MO, USA). Within 48 hours of arrival to the facility a physical

exam of each animal was performed to evaluate for lesions and to ensure normal heart and lung
sounds. A complete blood cell count and blood chemistry analysis were also performed. No pre-
treatment with any medications was performed.
All experiments were initiated during the morning hours. Animals were initially sedated
with 20mg/kg intramuscular ketamine; general anesthesia was subsequently induced and
mechanical ventilation initiated (Fabius GS; Draeger-Siemens, New York, NY) with a mixture of
60% oxygen and isoflurane (1-2.5%) with a tidal volume of 10mL/kg at a respiratory rate of 12
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min-1. End-tidal CO2 (ETCO2) was monitored by in-line waveform capnography, and the
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respiratory rate was adjusted to maintain an ETCO2 between 38 and 42 mm Hg prior to
induction of cardiac arrest. Continuous cardiac rhythm and heart rate were monitored by
electrocardiography (ECG) using standard limb leads. Peripheral capillary pulse oximetry
(SpO2) was also monitored continuously. The anesthesia used in this experiment is standard for
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swine models. All other drugs, routes of administration, and timing of administration are those
outlined in CPR guidelines (20, 21). Standard weight based doses were used.
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Interventions
High fidelity, solid state micromanometer-tipped pressure transducers (Millar MPC-500;

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Millar Inc., Houston, TX) were advanced through right internal jugular vein and right femoral
artery into thoracic locations to measure continuous aortic and right atrial pressures respectively.
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Unfractionated heparin (100u/kg) was provided to prevent catheter clotting. Near infrared
spectroscopy (NIRS) sensors were adhered to the scalp and the right flank to continuously
monitor and record cerebral and renal regional oximetry (rSO2) respectively (INOVS 5100C
Cerebral/Somatic Oximeter; Covidien, Minneapolis, MN). Once all catheters and sensors were

in place, the animals were allowed to acclimate for 10 minutes, and each animal received a bolus
of 15 mL/kg of 0.9% saline intravenously to replace overnight fasting fluid deficits.
Animals were placed in a v-shaped trough to eliminate lateral movements during chest
compressions. At the onset of the 10-minute acclimatization period inhaled oxygen was
decreased to 21%. During the 10-minute acclimatization period, transthoracic echocardiography
(TTE) (z.one ultra sp; Zonare Medical Systems, Inc., Mountain View, CA) was used to locate the
aortic root (AR) and the center of the LV in two orthogonal planes (the parasternal long axis and
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parasternal short axis). The animals’ skin was marked in the mid-sternum at the level of the AR
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to represent the traditional compression location and at the center of the LV to represent the LV
compression location. A multiplane transesophageal (TEE) transducer (P8-3TEE; Zonare
Medical Systems, Inc., Mountain View, CA) was used to obtain a mid-esophageal long axis (ME
LAX) view of the heart. The TEE transducer was left in place for recording the area of maximal
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compression (AMC) during compressions.
Experimental Protocol
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Animals were randomly allocated to LV or traditional chest compression groups prior to
the beginning of the study and the allocation results for each animal were kept sealed until
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ventricular fibrillation (VF) had been induced for each animal. A graphic display of the general
protocol is presented in Figure 1a, and a more detailed outline of the advanced life support
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(ALS) portion of the protocol is presented in Figure 1b.
During the hemorrhage period, 30% of each animals’ blood volume was removed over a
20-minute period, as previously described, at a rate of 1.42 ml/kg/min for the first 7 minutes
followed by a rate of 0.76 ml/kg/min over the remaining 13 minutes (22, 23). Blood was
removed from the carotid arterial line via aspiration with a 60mL syringe and saved in a blood

collection system containing citrate-phosphate-dextrose with Optisol red blood cell preservative
solution (Terumo Corp., Tokyo, Japan). The collected blood was then placed in a blood warmer
for subsequent experimental transfusion to the same animal.
Ventricular fibrillation (VF) was induced five minutes after the completion of
hemorrhage to simulate TCPA. VF was induced with a 3second 60Hz 100mA electric current
delivered across the thorax (Model 1745A Power Supply; B&K Precision Corporation, Yorba
Linda, CA) as previously described (24, 25). The induction of cardiac arrest represented time
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zero during the experiment; mechanical ventilation and anesthesia were simultaneously
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discontinued at time zero. All animals remained in VF arrest without any intervention for a
period of 10 minutes. During the 10-minute arrest period, the allocation to either the traditional
or LV compression groups was unblinded, and the center of the piston on the automatic
mechanical compression device (AMCD) (Thumper 407CC; Michigan Instruments, Grand

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Rapids, MI) was lowered into place over the corresponding skin marking. Defibrillation pads
were placed over the right and left lateral chest and connected to a biphasic electronic
defibrillator/monitor (Lifepak 20; Physio Control Inc., Redmond, WA).

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Basic Life Support

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After 10 minutes of cardiac arrest, Basic Life Support (BLS), was initiated using the
AMCD over the allocated position; compressions were delivered at a rate of 100 min-1, at a depth
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of 5cm, with a 50% duty cycle and a compression-ventilation ratio of 30:2. Compressions were
briefly interrupted every two minutes to perform a rhythm analysis that lasted 2-5 seconds.
During BLS, a 10 second video clip of the ME LAX view was saved for future review.
Although the use of automated external defibrillators (AED) has been incorporated into BLS
algorithms, a 10-minute interval of BLS without defibrillation was used as a practical approach
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because this duration of CPR is necessary to adequately compare CPR techniques (25).
Additionally, most bystanders do not have access to an AED and emergency medical services
(EMS) response times can approach or exceed 10 minutes, which allowed our BLS period to
approximate bystander BLS prior to the arrival of ALS qualified personnel (26-28).
Advanced Life Support
After 10 minutes of BLS, advanced life support was initiated with a 125 Joule (J)
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(approximately 4J/kg) biphasic waveform defibrillation attempt, resumption of mechanical
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ventilation with 100% oxygen, continuous compressions at the same rate and depth, and bolus
transfusion of 500mL of whole blood under 250mmHg of pressure (Figure 1b). We elected to
transfuse whole blood (WB) since WB is the resuscitation fluid that plasma, packed red blood
cells and platelets in a 1:1:1 ratio attempt to simulate, and fresh WB may be administered in
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tactical field care or elsewhere in combat theater when other blood products are not available or
not effective. (29, 30). Every two minutes, compressions were interrupted for a rhythm analysis
that lasted 2-5 seconds. If the rhythm was VF or VT, another 125J defibrillation attempt was
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provided and compressions were re-initiated. If the animal was in asystole or an organized
rhythm, no defibrillation attempt was made and compressions were re-initiated; if an organized
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rhythm was present at a second consecutive rhythm analysis, compressions were only re-initiated
if the animal did not meet criteria for ROSC. At the second and fourth ALS rhythm analyses,
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epinephrine (0.01mg/kg) followed by a 10mL normal saline flush was administered if the animal
had not met criteria for ROSC. During the third and fifth ALS rhythm analyses, amiodarone
(5mg/kg) followed by a 10mL normal saline flush was administered if the animal had not met
criteria for ROSC and was in a defibrillation-appropriate rhythm (VF or VT).
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Return of Spontaneous Circulation and Post-Resuscitation Care
Return of spontaneous circulation was defined as an organized rhythm with a sustained
aortic systolic blood pressure greater than 60 mm Hg without any intervention for one minute
during a scheduled rhythm check. If ROSC was attained, the animals were supported in a
simulated intensive care setting until termination of the protocol at minute 60. After ROSC,
mechanical ventilation was provided with the initial ventilator settings and 100% oxygen.
Respiratory rate was adjusted to maintain an ETCO2 of 38–42 mmHg. Inhales isoflurane was
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administered as necessary.
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An epinephrine infusion was started as needed, at a rate of 0.1mcg/kg/min and titrated by
0.1mcg/kg/min every two minutes to a maximum of 2.0mcg/kg/min, to maintain an aortic
systolic blood pressure (SBP) greater than 90mmHg. If the SBP rose above 120mmHg the
epinephrine was titrated down by 0.1mcg/kg/min every two minutes. An amiodarone infusion
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(5mg/kg/hr) was started if the animal had received amiodarone during ALS.
Termination of the Protocol

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Animals were considered expired if the aortic SBP was less than 60 for 10 minutes after
minute 30. Expired animals were euthanized with 100mg/kg sodium pentobarbital, and
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mechanical ventilation was terminated. Animals that did attain ROSC were supported until
minute 60, to ascertain short-term viability; at this time all life support, including medication
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infusions and mechanical ventilation, were terminated and the remaining animals were
euthanized. No post-care was performed as all animals were euthanized at the end of the study.
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Measurements
Hemodynamic data (aortic systolic and diastolic blood pressure, right atrial systolic and
diastolic blood pressure, SpO2, ETCO2, cerebral and renal regional oximetry) were continuously
monitored; the two-minute intervals at the end of each experimental period (baseline, post-
hemorrhage, end of non-intervention, end of BLS, end of ALS) were averaged and analyzed.
Baseline for hemodynamic measurements was defined as the two-minute interval immediately
prior to hemorrhage. Post-hemorrhage was defined as the two-minute interval immediately prior
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to time zero. End of non-intervention was defined as the two-minute interval immediately prior
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to initiation of BLS (systolic and diastolic blood pressures as well as SpO2 were not measurable
during the non-intervention period). CPP was calculated as the difference between the end-
diastolic aortic pressure and the simultaneous end-diastolic right atrial pressure.
Arterial blood gas (ABG) specimens were obtained at baseline (immediately prior to
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hemorrhage), post-hemorrhage (immediately prior to time zero), end of non-intervention, end of
BLS, and end of ALS during the protocol.
The number of animals that attained ROSC in each group and the number of ROSC
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animals that survived to 60 minutes was subsequently recorded. The total amount of epinephrine
and amiodarone that each animal received were also recorded.

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The ten second TEE video recordings were randomly compiled into a file that was
independently assessed at the conclusion of all data collection by an investigator who is certified
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in TEE and blinded to the remainder of the data. This investigator rated the AMC in each video
as being over the LV or AR.
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Outcomes
The primary outcome was the difference in ROSC between the two experimental groups.
Secondary outcomes included the difference in: 1) short-term, 60-minute survival, 2)
hemodynamic variables, and 3) ABG variables between the traditional and LV groups.
Analysis
Means and standard deviations were calculated for measured variables of each treatment
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group across all time intervals. Shapiro-Wilk tests were used to test for normality. The treatment
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groups were compared on baseline weight and size, as well as the total amount of amiodarone
and epinephrine administered using the nonparametric Wilcoxon/Mann-Whitney test.
Differences in rates of survival were analyzed using Fisher's exact test. To control for within-
subject variation (due to repeated measures over time) and between-subject variation (due to
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different treatment groups), a two-way repeated measures analysis of variance (ANOVA) was
performed for the hemodynamic and ABG variables. The Greenhouse-Geisser correction was
used to correct for violations of the assumption of sphericity, and the Bonferroni correction was
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applied for multiple comparisons. Statistical significance was defined as p<0.05, and 95%
confidence intervals were provided.

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Regarding sample size, based on protocol development data, 43% of animals were
expected to attain ROSC (primary outcome) in the LV compressions and 0% in the traditional
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group; at the α = 5% significance level and with 80% power, a total sample size of 26 animals
would be required.
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RESULTS
There was no difference in the size of the animals or the baseline hemodynamic and
laboratory measures between the traditional and LV groups (p>0.05 for all measures) (Table 1).
The mean total dose of epinephrine was similar between the LV (0.38mg ± 0.25mg SD) and
traditional group (0.47 ± 0.24mg SD) (95%CI -0.10-0.29). The mean total dose of amiodarone
was higher in the traditional group (257mg ± 87.7mg SD) compared to the LV group (155mg ±
133mg SD) (95% CI 9.56-193). There was 100% agreement between the AMC by TEE review
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and location of AMCD placement (κ =1.0, 95% CI 1.0-1.0).
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Return of Spontaneous Circulation and Short-term survival
The number of animals that attained ROSC was significantly higher in the LV group
(p=0.0391) (Table 2). All five animals that attained ROSC did so during the ALS period (two at
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minute 22, one at minute 24, one at minute 26, and one at minute 28), and all animals that
attained ROSC survived to 60 minutes.

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Hemodynamic and Laboratory Variables
The difference in the hemodynamic variables between the LV and traditional experimental
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groups are demonstrated in Table 3. The differences in the mean blood gas analysis variables
between the LV and traditional experimental groups are demonstrated in Table 4. Detailed
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graphical representation of hemodynamic values across the entire resuscitative period are
presented in Appendix 1 (see Appendix, Supplemental Digital Content 1,
http://links.lww.com/TA/B127).
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DISCUSSION
In our study, we detected a difference in ROSC and hemodynamics when chest
compressions are performed in two different locations in a swine model of traumatic cardiac
arrest. Most notably, there was an increase in Aortic SBP, Aortic DBP and CPP at the end of
both the BLS and ALS resuscitation periods among the LV group.
In most instances, performing chest compressions directly over the LV during TCPA may
be the closest approximation to open chest compressions available in the pre-hospital setting.
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Recent studies have indicated that the current traditional location for chest compressions, “on the
center (middle) of the victim’s chest” is not optimal because the heart is not located beneath this
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location, the thorax is more compressible caudally, and hemodynamic measures, including
diastolic arterial pressures, increase when compressions are performed at the lower end of the
sternum, more directly over the heart, rather than at the traditional location (20, 21, 31-33). The
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increase in diastolic arterial pressures with distal compressions is of interest since increases in
Aortic DBP and CPP have repeatedly been shown to be correlated with cardiac output and
myocardial blood flow (34-36). Our group previously demonstrated that CPP and ROSC can be
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improved by placing chest compressions directly over the left ventricle in non-traumatic cardiac
arrest (18). In this traumatic arrest model we used an identical cardiac arrest protocol, however,
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we hemorrhaged the animals prior to inducing VF to evaluate whether the improvements in
hemodynamics and ROSC could be maintained in a hypovolemic state; although we only

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induced Class III shock prior to inducing VF in this traumatic arrest model, our results
demonstrate that the hemodynamic and ROSC improvements seen in the medical arrest model do
indeed remain in a hypovolemic state.
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In our experiment the higher rate of ROSC among the LV group is most likely due to an
increase in CPP during the BLS interval. Appendix 1E demonstrates that animals in the LV
group maintained a higher average CPP than the traditional group (see Appendix 1E,
Supplemental Digital Content 1, http://links.lww.com/TA/B127). This observation highlights
the importance of meeting a minimum threshold CPP to attain ROSC. Both human and animal
investigations have demonstrated a strong association between CPP and resuscitation outcomes
(24, 36-38). Failure to generate a CPP of at least 15–20 mm Hg during CPR is rarely associated
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with successful resuscitation (24, 37, 39). Our study illustrates that the threshold CPP for ROSC
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is more likely to be met when chest compressions are performed directly over the LV. This is an
important finding since it has been reported that chest compressions are ineffective in trauma
associated with low LV end diastolic volumes; our findings demonstrate that compressions in the
standard location may not be sufficiently effective, however, compressions over the LV are able
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to produce sufficient CPP to attain ROSC even in a hypovolemic state (40).
Our study highlights the importance that the location of chest compressions has in
attaining ROSC during TCPA. Since ROSC was only attained in the LV group of our animal
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experiment, it is possible that the survival rate for humans receiving CPR is dismally low
because the only survivors are those few individuals whose hearts lie closer to the center of the
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chest where rescuers are traditionally performing compressions. For our results to become
clinically relevant, these findings must be made applicable to the first providers who are
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performing CPR during the most time-sensitive period of resuscitation. There may simply be a
more optimal landmark than the “center of the chest,” however, individual anatomy varies
greatly and a single landmark is not likely to be optimal in every case. For first responders and
hospital personnel, more advanced technology is already available and may be further developed
to aid in locating the ideal location for compressions. Some prehospital providers are already
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facile with limited ultrasound modalities and could likely reproduce the same simple TTE
techniques we used to locate the left ventricle in this animal study (41). More scientific work is
needed to identify the potential solutions that should be used by prehospital providers in
identifying the optimal location for chest compressions.
Limitations
First, this animal model does not precisely replicate the human experience during cardiac
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arrest. Swine are often used in cardiac arrest studies due to the cardiovascular and metabolic
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similarities to humans, however, the swine heart is more vertically oriented, there is an extra lobe
of lung in the left hemithorax and there are differences in chest wall anatomy which somewhat
alter compression mechanics (42-45). In the average human, compression directly over the left
ventricle would likely occur even more laterally on the chest that in swine. None of these
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anatomic differences diminish the importance of the finding that chest compressions in different
locations on the chest alter the rate of ROSC and hemodynamic variables. Additionally, we
analyzed young healthy swine which may which may not be physiologically similar to some
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TCPA patients; however, although trauma is the fourth leading cause of death overall for all ages
in humans, trauma is also the leading cause of death for humans ages 1-44 suggesting that a
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young swine model is likely more reflective of human physiology than an older swine model (5).
There is also evidence for sex differences in the magnitude of cardiac and cerebral injury after
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hemorrhage and ventricular fibrillation, so generalization to males may not be possible (46).
Second, in our experiment we induced VF arrest during class III hemorrhage which may not
cause TCPA in many instances. This was done to limit the number of animals needed to
determine if there is a difference in hemodynamics and ROSC after hemorrhage and VF. Further
work is being done to determine if these differences persist in class IV hemorrhage. Third, only
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short-term survival to 60-minutes post-arrest was evaluated in ROSC animals. Further
investigation into long-term survival and neurologic outcomes needs to be performed, however,
long-term survival is only possible when short-term survival has been achieved. In this study, if
the animals began to demonstrate any movement during the survival period they were sedated,
and sedation was not an outcome that we measured. At this time, it is still unclear whether long-
term survival and neurologic outcomes can be improved by enhancing hemodynamics with LV
compressions. Finally, this study only addressed VF as the initial cardiac rhythm after inducing
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hemorrhagic shock. Pulseless electrical activity (PEA) is the most common cardiac rhythm in
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TCPA, however, both PEA and VF have higher survival rates from TCPA than asystole. It is
also possible that the results may vary with PEA or asystole as the initial rhythm, however, we
chose to use VF in our model to maintain uniformity between this study and our prior non-
traumatic cardiac arrest study (18). Ventricular fibrillation also ensured that our animals were
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truly in a cardiac arrest state rather than simply in a severe hemorrhagic shock state without
palpable pulses which is likely the case with many traumatic PEA models where the most
beneficial treatment is the transfusion of blood.

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CONCLUSION
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Closed chest compressions directed over the LV resulted in higher rate of ROSC and short-
term survival compared to chest compressions in the traditional location in a swine model of
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TCPA. Additionally, there was an increase in Aortic SBP, Aortic DBP and CPP at the end of
both the BLS and ALS resuscitation periods among the LV group. These improvements in
hemodynamics likely contributed to the higher rates of ROSC and short-term survival.
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AUTHORSHIP
K.L.A., K.C.F. and V.S.B. conceived and designed the trial. K.L.A. and V.S.B. obtained research
funding. M.G.C. and S.M.B. performed the experiments. K.L.A. supervised the conduct of the
study and data collection. A.A.A provided statistical advice on study design and analyzed the
data. K.L.A. and V.S.B. drafted the manuscript; all authors contributed substantially to
manuscript revision, then read and approved the final article.
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DISCLOSURE
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Competing Interests. None of the authors have any conflicts of interest to disclose.
Funding. This study was funded by a grant from the Office of the Air Force Surgeon General.
Disclaimer. The views expressed in this manuscript are those of the authors and do not reflect
official policy or position of the United States Government, Department of Defense, or the
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United States Air Force.
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FIGURE LEGENDS
FIGURE 1. (a) Experimental protocol timeline; (b) Detailed ALS protocol timeline. *=rhythm
check, BLS=Basic Life Support, ALS=Advanced Life Support, Post Resusc=Post Resuscitation,
t=time, VF=ventricular fibrillation, ROSC=return of spontaneous circulation, J=joules,
CPR=cardiopulmonary resuscitation, FiO2=fraction of inspired oxygen, mg-milligram,
kg=kilogram, Epi=epinephrine, Amio=amiodarone, prn=as needed, gtt=infusion.
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Table 1. Baseline weight and size of animals
Traditional LV
(n=13) (n=13)
Weight (kg) 29 (2.1) 28 (2.5)
Vertical distance from sternal notch to aortic root (cm) 5.5 (0.75) 6.1 (3.1)
Vertical distance from sternal notch to mid LV (cm) 11 (0.95) 10 (3.1)
Lateral distance from sternum to mid LV(cm) 3.0 (0.38) 3.9 (2.5)
Data presented as mean (SD). No significant differences exist between groups on any of the listed
measures at p<0.05. LV=left ventricle, kg=kilogram, cm=centimeter
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Table 2. Rates of ROSC and Short-term survival
Traditional LV Relative
95% CI p-value
(n=13) (n=13) Risk
ROSC 0 5 (38%) 0.62 0.40-0.95 0.04
Survival to 60 minutes 0 5 (38%) 0.62 0.40-0.95 0.04
Data are presented as n (%). LV=left ventricle, CI=confidence interval
Fisher’s exact test used to determine p-value
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Table 3. Results of Repeated Measures ANOVAs for Hemodynamic Variables
Traditional LV 95% CI of difference p-value

(n=13) (n=13) LL UL
AoS (mmHg)
Baseline 100 (14.6) 101 (5.68) -9.38 8.54 0.923
Post-hemorrhage 57.0 (13.4) 63.3 (14.1) -17.0 4.46 0.240
End of BLS 30.3 (6.67) 65.2 (24.1) -49.2 -20.6 <0.001*
End of ALS 41.1 (10.2) 85.0 (37.9) -66.3 -21.4 <0.001*
AoD (mmHg)
Baseline 61.1 (13.1) 62.5 (6.08) -9.66 6.89 0.733
Post-hemorrhage 33.1 (6.83) 38.6 (8.73) -11.9 0.85 0.086
End of BLS 8.19 (3.77) 17.9 (6.16) -13.8 -5.56 <0.001*
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End of ALS 12.7 (3.31) 40.5 (36.4) -48.7 -6.84 0.011*
RAS (mmHg)
Baseline 4.46 (3.63) 4.04 (3.28) -2.38 3.23 0.758
Post-hemorrhage 3.96 (4.15) 1.73 (2.95) -0.68 5.14 0.127
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End of BLS 38.8 (9.85) 110 (43.2) -96.2 -45.5 <0.001*
End of ALS 47.7 (11.9) 82.1 (65.8) -72.7 3.88 0.076
RAD (mmHg)
Baseline -0.92 (3.49) -1.15 (3.29) -2.52 2.98 0.864
Post-hemorrhage -1.65 (4.84) -3.46 (3.45) -1.60 5.21 0.284
End of BLS -1.46 (4.12) -2.92 (4.31) -1.95 4.88 0.386
End of ALS 3.35 (4.21) 1.81 (4.37) -1.93 5.01 0.370
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CPP (mmHg)
Baseline 62.0 (13.8) 63.6 (7.08) -10.5 7.27 0.711
Post-hemorrhage 34.8 (7.43) 42.1 (9.01) -14.0 -0.62 0.033*
End of BLS 9.65 (4.48) 20.8 (4.70) -14.9 -7.44 <0.001*
End of ALS 9.39 (3.76) 38.7 (37.9) -51.1 -7.54 0.010*
SpO2 (mmHg)
Baseline 97.2 (2.28) 96.8 (1.23) -1.39 2.20 0.635
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Post-hemorrhage 97.8 (1.60) 97.1 (2.56) -1.98 3.33 0.596

End of BLS 73.1 (4.22) 80.1 (8.77) -15.9 1.85 0.112
End of ALS 75.0 (4.80) 83.4 (12.7) -21.0 4.28 0.178
ETCO2 (mmHg)
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Baseline 41.9 (4.04) 38.8 (0.57) -0.83 7.00 0.114

Post-hemorrhage 39.0 (4.57) 37.8 (2.77) -3.52 5.84 0.606
End non-intervention 12.2 (8.95) 12.9 (3.13) -6.66 5.13 0.791
End of BLS 47.1 (12.30) 48.0 (8.12) -13.6 11.8 0.880
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End of ACLS 18.5 (4.52) 23.8 (9.16) -12.1 1.36 0.110

cerebral rSO2 (%)
Baseline 61.3 (5.04) 65.2 (9.01) -9.84 2.12 0.195
Post-hemorrhage 50.6 (7.83) 51.3 (10.82) -8.49 7.05 0.850
End of BLS 25.1 (10.78) 28.9 (10.36) -12.6 4.92 0.374
End of ALS 24.2 (10.73) 37.3 (22.2) -27.4 1.16 0.070
renal rSO2 (%)
Baseline 66.3 (2.96) 66.9 (4.39) -3.64 2.62 0.738
Post-hemorrhage 63.3 (2.77) 62.3 (5.01) -2.44 4.34 0.568
33

Traditional LV 95% CI of difference p-value
(n=13) (n=13) LL UL
End of BLS 49.3 (5.66) 47.7 (5.11) -2.90 6.01 0.477
End of ALS 49.1 (5.76) 54.3 (14.9) -14.7 4.27 0.267
Data presented at mean (SD). LV=left ventricle, CI=confidence interval, LL=lower limit, UL=upper limit,
Ao=aortic, RA=right atrial, S=systolic blood pressure, D=diastolic blood pressure, mmHg=millimeters of
mercury, BLS=basic life support, ALS=advanced life support, SpO2=peripheral capillary oxygen
saturation, ETCO2= end-tidal capnography, rSO2=regional oximetry. *=significant difference, p<0.05;
adjusted p-values for repeated measures ANOVA are reported.
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Table 4. Results of Repeated Measures ANOVAs for Arterial Blood Gas Variables
95% CI of
Traditional LV p-value
difference
(n=13) (n=13)
LL UL
pH
Baseline 7.48 (0.04) 7.47 (0.04) -0.03 0.03 0.753
Post-hemorrhage 7.48 (0.03) 7.48 (0.03) -0.03 0.03 0.953
End of BLS 7.27 (0.13) 7.14 (0.15) 0.02 0.24 0.027*
End of ALS 7.24 (0.12) 7.18 (0.12) -0.03 0.17 0.175
pCO2
Baseline 39.9 (4.84) 39.4 (3.00) -2.77 3.76 0.758
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Post-hemorrhage 38.0 (4.74) 35.4 (3.92) -0.86 6.18 0.132
End of BLS 48.5 (12.2) 67.6 (26.1) -35.8 -2.49 0.026*
End of ALS 37.5 (8.97) 51.9 (18.6) -26.2 -2.56 0.019*
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pO2
Baseline 195 (22.6) 186 (54.1) -24.6 42.6 0.585
Post-hemorrhage 207 (19.8) 198 (47.9) -20.4 39.0 0.526
End non-intervention 96.67 (22.4) 110 (17.4) -30.0 2.44 0.092
End of BLS 187 (92.4) 131 (70.0) -10.3 122 0.094
End of ALS 179 (119) 140 (128) -61.3 139 0.432
Data presented as mean (SD). LV=left ventricle, CI=confidence interval, LL=lower limit, UL=upper limit,
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pCO2=partial pressure of carbon dioxide, pO2=partial pressure of oxygen, BLS=basic life support,
ALS=advanced life support, *=significant difference, p<0.05; adjusted p-values for repeated measures
ANOVA are reported.
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Appendix 1 Hemodynamics
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Journal of Trauma and Acute Care Surgery, Publish Ahead of Print

Left Ventricular Compressions Improve Return of Spontaneous Circulation

and Hemodynamics in a Swine Model of Traumatic Cardiopulmonary Arrest

Stanford University School of Medicine

900 Welch Road, Ste 350

Madigan Army Medical Center

9040 Jackson Ave

CREST Research Program

Wilford Hall Ambulatory Surgical Center

2200 Bergquist Dr.

Lackland AFB, TX 78236

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

CREST Research Program

Wilford Hall Ambulatory Surgical Center

2200 Bergquist Dr.

Lackland AFB, TX 78236

Allyson A. Araña, PhD

3551 Roger Brooke Drive

Fort Sam Houston, TX 78234

University of Colorado School of Medicine

Department of Emergency Medicine

12401 East 17th Avenue, Campus Box L10, Rm 751

CONFLICT OF INTEREST STATEMENT:

None of the authors have any conflicts of interest to disclose.

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

Fort Lauderdale, Florida.

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

Background: Prehospital cardiopulmonary resuscitation, including closed chest compressions,

hemodynamics when compared to traditional compressions. We hypothesized that chest

swine model of traumatic cardiopulmonary arrest (TCPA).

two minutes of BLS and ALS periods.

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

Level of Evidence: Therapeutic Animal Model, Level I

Keywords: Cardiopulmonary resuscitation; Trauma; Hemodynamics; Survival;

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

Resuscitation of traumatic cardiopulmonary arrest (TCPA) patients in the pre-hospital

and an inappropriate utilization of resources (1-4). In 2003 the National Association of

Trauma established guidelines regarding the withholding or termination of out-of-hospital

Cardiopulmonary resuscitation, including closed chest compressions, has commonly been

hemodynamics and survival when applied to TCPA.

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

would increase return of spontaneous circulation (ROSC) when compared to traditional

compressions in a swine model of TCPA. Secondary analyses included an evaluation of

Reporting In Vivo Experiments (ARRIVE) guidelines. (19)

viral, bacterial and parasitic pathogens.

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

treatment with any medications was performed.

High fidelity, solid state micromanometer-tipped pressure transducers (Millar MPC-500;

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

of 15 mL/kg of 0.9% saline intravenously to replace overnight fasting fluid deficits.

decreased to 21%. During the 10-minute acclimatization period, transthoracic echocardiography

compression location. A multiplane transesophageal (TEE) transducer (P8-3TEE; Zonare

Animals were randomly allocated to LV or traditional chest compression groups prior to

(ALS) portion of the protocol is presented in Figure 1b.

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

for subsequent experimental transfusion to the same animal.

mechanical compression device (AMCD) (Thumper 407CC; Michigan Instruments, Grand

defibrillator/monitor (Lifepak 20; Physio Control Inc., Redmond, WA).

Basic Life Support

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

Advanced Life Support

criteria for ROSC and was in a defibrillation-appropriate rhythm (VF or VT).

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.