American Journal of Emergency Medicine 33 (2015) 1385–1390
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American Journal of Emergency Medicine
journal homepage: www.elsevier.com/locate/ajem
Original Contribution
Prearrest hypothermia improved defibrillation and cardiac function in a
rabbit ventricular fibrillation model☆
Li Jiang, MM a,d,1, Chun-lin Hu, MD b,1, Zhen-Ping Wang, BMed c, Yin-Ping Li, MM d, Jian Qin, MD d,⁎
a
Department of Emergency Medicine, Third Military Medical University Affiliated XinQiao Hospital, Chongqing, China
Department of Emergency Medicine, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
Department of General Surgery, JiNan Central Hospital, JiNan, ShanDong, China
d
Department of Emergency Medicine, Capital Medical University Affiliated XuanWu Hospital, Beijing, China
b
c
a r t i c l e
i n f o
Article history:
Received 20 January 2015
Received in revised form 11 June 2015
Accepted 7 July 2015
a b s t r a c t
Background: Hypothermia when cardiopulmonary resuscitation begins may help achieve defibrillation and return of spontaneous circulation (ROSC), but few data are available.
Objective: The objective of this study was to determine whether prearrest hypothermia improved defibrillation
and cardiac function in a rabbit ventricular fibrillation (VF) model.
Results: Thirty-six New Zealand rabbits were randomized equally to receive normothermia (Norm) (~ 39°C),
post-ROSC hypothermia (~33°C), or prearrest hypothermia (~33°C). Ventricular fibrillation was induced by alternating current. After 4 minutes of VF, rabbits were defibrillated and given cardiopulmonary resuscitation
until ROSC or no response (≥30 minutes). Hemodynamics and electrocardiogram were monitored; N-terminal
pro–brain natriuretic peptide and troponin I were determined by enzyme-linked immunosorbent assay. Myocardial histology and echocardiographic data were evaluated. First-shock achievement of perfusion rhythm was
more frequent in prearrest than normothermic animals (7/12 vs 1/12; P = .027). After ROSC, dp/dtmax was higher
in prearrest than normothermic animals (P b .001). Left ventricular end-systolic pressure was higher in prearrest
than normothermic animals (P = .001). At 240 minutes after ROSC, troponin I and N-terminal pro–brain natriuretic peptide were lower in prearrest than normothermic animals (15.74 ± 2.26 vs 25.09 ± 1.85 ng/mL and
426 ± 23 vs 284 ± 45 pg/mL, respectively), the left ventricular ejection fraction and cardiac output were
lower in the Norm group than other 2 groups (P b .01). Myocardial histology was more disturbed in normothermic than post-ROSC and prearrest animals, but was not different in the latter 2 groups.
Conclusions: Induction of hypothermia before VF led to improved cardiac function in a rabbit VF model through
improving achievement of perfusing rhythm by first-shock defibrillation and facilitating resuscitation.
© 2015 Published by Elsevier Inc.
1. Introduction
Cardiovascular disease (CVD) is the leading cause of death and disability in most industrialized nations. In China, CVD morbidity and mortality are increasing annually along with both standard of living and
poor lifestyle habits. Currently in China, CVD causes about 60% of sudden
cardiac deaths, making it a serious clinical and public health problem.
☆ This study was supported by funding from CPR New Theory, New Technology in Improving Cardiac Arrest Resuscitation Success Rate (xm201313). The funders had no role
in the study design, data collection, analysis, decision to publish, or the preparation of
the manuscript.
⁎ Corresponding author at: Department of Emergency Medicine, Capital Medical University Affiliated XuanWu Hospital, Beijing 100053, China. Tel.: +86 13910183721;
fax: +86 10 83198382.
E-mail address: jqin6@163.com (J. Qin).
1
These 2 authors contributed equally to this work.
http://dx.doi.org/10.1016/j.ajem.2015.07.017
0735-6757/© 2015 Published by Elsevier Inc.
Therapeutic hypothermia has been used for treatment of critical illnesses, including traumatic brain injury [1], refractory arrhythmias [2],
cardiogenic shock syndrome [3], and decrease of infarct size in patients
undergoing percutaneous coronary intervention for acute myocardial infarction [4] for more than 50 years. Systemic hypothermia initiated after
cardiac arrest and resuscitation can improve survival and long-term neurologic outcome [5,6], but there are few data on the heart effects.
The American Heart Association 2010 guidelines for cardiopulmonary resuscitation (CPR) recommend that comatose adult patients
with out-of-hospital ventricular fibrillation (VF) and cardiac arrest be
cooled to 32°C to 34°C for 12 to 24 hours after return of spontaneous circulation (ROSC). However, many unanswered questions remain, including the optimal timing for hypothermia [7].
Animal studies that induced intra-arrest or prearrest hypothermia
with cooling at approximately the same time as defibrillation and CPR
reported improved defibrillation or ROSC [8–14]. However, only a few
studies have reported the effects of preexisting hypothermia on resuscitation and myocardial function. Additional data are needed to find ways
to optimize the effectiveness of CPR.
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L. Jiang et al. / American Journal of Emergency Medicine 33 (2015) 1385–1390
In this study, prearrest and post-ROSC systemic hypothermia were induced in a rabbit VF model to determine whether prearrest hypothermia
has a cardiac function benefit. Hemodynamic function, troponin I, and Nterminal pro–brain natriuretic peptide (NT-proBNP) levels, echocardiography, and cardiac tissue histology of the animals were monitored.
2. Materials and methods
2.1. Animal preparation
Thirty-six male New Zealand rabbits weighing 2.8 to 3.5 kg were
maintained under standard laboratory conditions. Anesthesia was induced with 30.0 mg/kg pentobarbital (Sigma, St Louise, MI); supplemental pentobarbital was given as required to maintain sedation. The
animals were intubated and ventilated (45 breaths/min, 15 mL/kg). Arterial blood gases were monitored; physiological arterial blood pH and
PO2 N 100 mm Hg were maintained by ventilation adjustments. Catheters were inserted into the femoral artery and ear marginal vein to monitor arterial blood pressure and administer medications. A pressure
catheter (Kombidyn Monitoring Set, Braun, Melsungen, Germany) introduced into the left ventricle through the right carotid artery measured end diastolic and systolic pressures and the rates of positive
(dp/dtmax) and negative (dp/dtmin) development. Hemodynamics and
electrocardiogram (ECG) were monitored with an MP150 data acquisition system (version 3.8.1; Biopac, Goleta, CA).
2.2. Induction of hypothermia
Animals were randomized to 3 treatment groups of equal size: normothermia (~39°C, Norm), cooling to ~33°C after ROSC (post-ROSC), or
cooling to ~ 33°C before VF with maintenance of hypothermia after
achieving ROSC (prearrest). Rabbits were cooled by placing ice bags
around the head, thorax, and abdomen. The bags were removed when
body temperature fell to within 0.4°C or 0.5°C above target because it
continued to fall for a brief time afterward. Cooling to 34°C required
28.3 ± 3.5 minutes, ice and electric heating pads were used to maintain
animals at target temperature, and rectal temperature was monitored
using probes supplied with the MP150 system (Biopac). All procedures
described above were completed in less than 1 hour.
2.3. Ventricular fibrillation and resuscitation
Fine acupuncture needles were placed in the ventricular apex of the
myocardium and the right thoracic subcutis. A 6-V, 50-Hz alternating
current, was applied to the acupuncture needles until VF was confirmed
by surface ECG accompanied by a fall in arterial blood pressure to near
zero. After 4 minutes of VF arrest without chest compression or ventilation, rabbits were defibrillated with a commercially available biphasic
waveform defibrillator (HP-1723B; Hewlett Packard, Palo Alto, CA).
The first shocks were given at 10 J. Cardiopulmonary resuscitation,
with chest compressions at ~ 200/min and mechanical ventilation at
45 breaths/min, was then begun. Chest compression was interrupted
for no more than 5 seconds every 30 seconds to observe the ECG and
measure arterial pressure. After 30 seconds, additional shocks were delivered at 30 J if needed. Epinephrine 20 μg/kg was given intravenously
every 3 minutes after the first shocks as needed for continuing hypotension (arterial pressure b50 mm Hg). Cardiopulmonary resuscitation was
continued until achieving ROSC, mean arterial pressure (MAP) greater
than 60 mm Hg without drug infusion or continued chest compressions
for 5 minutes, or no response after at least 30 minutes. No drugs
were given after ROSC. MAP, dp/dtmax, dp/dtmin, left ventricular enddiastolic pressure (LVEDP), and left ventricular end-systolic pressure
(LVESP) were measured using the MP150 system. Hypothermia was
maintained and hemodynamics were monitored continuously for 4
hours after ROSC. No liquids were given during the study. A flow diagram of the study procedures is shown in Fig. 1.
2.4. Blood samples
Blood was collected from the left ventricle at 4 hours after ROSC and
centrifuged (B160A medical centrifuge, Baiyang, China) to separate the
plasma. Plasma NT-proBNP and troponin I levels were determined by
enzyme-linked immunosorbent assay (R&D, Minneapolis, MN). Surviving animals were euthanized with 5 mL intravenous 10% KCl.
2.5. Cardiac function study by echocardiography
Echocardiography was performed with the aid of the M-Turbo
Ultrasound System with a 5- to 10-MHz transthoracic echocardiographic transducer (SonoSite, Bothell, WA) on all animals at baseline and 4
hours after the ROSC. Longitudinal and transverse parasternal and 4- and
2-chamber apical views were obtained. The M-mode, 2-dimensional, and
Doppler imaging were examined, and the internal dimensions were recorded. Left ventricular end-systolic (ESV) and end-diastolic volumes
(EDV) were calculated by the method of Simpson, and the left ventricular ejection fraction (EF) and cardiac output (CO) were estimated.
2.6. Myocardial histology
Hearts were excised immediately after the 4-hour observation
period. Tissue blocks were prepared from the free left ventricular
subendocardium. Briefly, tissue samples were fixed in cold 2.5%
glutaraldehyde in 0.1 mol/L cacodylate buffer (pH 7.4), postfixed in 1%
osmium tetroxide, dehydrated, and embedded in Epon. Random 60to 80-nm ultrathin sections were cut following stereological sampling
methods without consideration of the sectioning orientation, mounted
on copper grids, and stained with lead citrate and uranyl acetate. The
myocardial ultrastructure was examined using an FEI Tecnai G2 transmission electron microscope equipped with a CCD camera (Gatan 832,
Pleasanton, CA) at magnifications from 500 to 135 000. Eight electron
micrographs were obtained randomly and sequentially from 1 section
cut from a block of tissue from each animal [15].
2.7. Calculation
Descriptive data were reported as proportions and means ± SD, and
statistical analysis was performed with SPSS 16.0 (SSPS Inc, Chicago, IL).
The hemodynamic and echocardiographic variables were found to be
normally distributed; therefore, no transformation of data was needed
prior to analysis. For variables that were not normally distributed,
Fig. 1. A flowchart of the experimental protocol.
L. Jiang et al. / American Journal of Emergency Medicine 33 (2015) 1385–1390
nonparametric methods were used. A linear mixed-model repeatedmeasures analysis was used to compare heart rate (HR), MAP, dp/
dtmax, dp/dtmin, LVESP, and LVEDP at 30, 60, 120, 180, and 240 minutes
after ROSC. Dichotomous variables were compared with 2-tailed Fisher
exact and t tests. Continuous variables were compared by analysis of
variance. Defibrillation and resuscitation data were tested for significance by Fisher exact test. The total number of shocks and epinephrine
dosage delivered within each of the 3 groups were compared using the
Kruskal-Wallis test. For all statistical analyses, a P value less than .05 was
considered significant.
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Table 2
Defibrillation and resuscitation outcomes
First-shock success
First-shock perfusing rhythm
ROSC achieved
Norm
(n = 12)
Post-ROSC
(n = 12)
Prearrest
(n = 12)
5/12
1/12⁎
9/12
5/12
0/12⁎
8/12
8/12
7/12
11/12
⁎ P ≤ .05 vs prearrest.
3.3. Hemodynamic data
3. Results
3.1. Baseline
A total of 36 rabbits were randomized equally to the 3 treatment
groups, and their baseline characteristics are presented in Table 1.
There were no differences in baseline HR, MAP, dp/dtmax, dp/dtmin,
LVEDP, LVESP, body temperature, or echocardiographic data. Ventricular fibrillation was induced after induction of hypothermia in the
prearrest group or at an equivalent time in other 2 groups.
Heart rate and dp/dtmin were significantly lower the in the prearrest
group after cooling than those in the Norm and post-ROSC groups before cardiac arrest (Table 1). Differences in MAP, dp/dtmax, LVEDP, and
LVESP observed after cooling were not significant.
As shown in Table 3, HR was higher in the Norm group than in the
post-ROSC and prearrest groups (P b .001). There were no significant
differences in MAP or LVEDP among the groups. The prearrest group,
but not the post-ROSC group, had a higher dp/dtmax (P b .001) than
the Norm group. dp/dtmin was lower in the post-ROSC group than in
the Norm group (P = .001), but the difference in dp/dtmin in the
prearrest and Norm groups was not significant. Finally, LVESP was
higher in the prearrest than in the Norm group (P = .001).
3.2. Resuscitation data
3.4. Troponin I and NT-proBNP
Successful defibrillation was defined as termination of VF regardless
of asystole, pulseless electrical activity, or sinus rhythm. Defibrillation
and resuscitation outcomes are shown in Table 2. First-shock defibrillation, that is, termination of VF with the first 10-J shock, succeeded in 5 of
the 12 animals in the Norm group, 8 of 12 in the prearrest group, and 5
of 12 in the post-ROSC group. These differences were not statistically
significant, and there were also no differences in the total number of defibrillation shocks delivered in each group. Seven of the 12 animals in
the prearrest group achieved ROSC immediately after initial 10-J shocks
without CPR or drug support compared with 1 of 12 in the Norm group
(P = .027) and 0 of 12 in the post-ROSC group (P = .005). Nine of 12 animals in the Norm group, 8 of 12 in the post-ROSC group, and 11 of 12 in
the prearrest group achieved ROSC.
The median epinephrine dose administered in the prearrest
group (0 μg/kg; range, 0-680 μg/kg) was less than those in the
Norm group (66 μg/kg; range, 0-680 μg/kg; P b .05). There was no
significant difference in the median epinephrine doses given in the
post-ROSC (69 μg/kg; range, 58-700 μg/kg) and Norm groups.
Table 1
Data at baseline and after induction of hypothermia
Characteristic
Norm (n = 12) Post-ROSC (n = 12) Prearrest (n = 12)
Baseline
HR
312 ± 21
MAP (mm Hg)
100 ± 11
dp/dtmax (mm Hg/s) 3542 ± 437
dp/dtmin (mm Hg/s) 3066 ± 598
LVEDP (mm Hg)
−0.1 ± 2.0
LVESP (mm Hg)
118 ± 11
Temperature (°C)
38.9 ± 0.1
Before induction of VF
HR (beats/min)
291 ± 18
MAP (mm Hg)
96 ± 6
dp/dtmax (mm Hg/s) 3034 ± 422
dp/dtmin (mm Hg/s) 3129 ± 543
LVEDP (mm Hg)
1.1 ± 0.8
LVESP (mm Hg)
110 ± 13
Temperature (°C)
38.8 ± 0.2
Values are means ± SEM.
⁎ P ≤ .05 compared with Norm.
⁎⁎ P ≤ .05 compared with post-ROSC.
295 ± 26
96 ± 8
3402 ± 305
2769 ± 191
1.2 ± 3.0
119 ± 10
38.9 ± 0.1
293 ± 21
102 ± 10
3413 ± 356
2939 ± 466
1.1 ± 1.9
123 ± 12
39.0 ± 0.2
300 ± 16
97 ± 6
2932 ± 341
2909 ± 258
2.1 ± 1.6
106 ± 17
38.8 ± 0.1
211 ± 16⁎,⁎⁎
96 ± 14
3052 ± 225
2278 ± 362⁎,⁎⁎
1.6 ± 1.5
106 ± 12
33.3 ± 0.1⁎,⁎⁎
Prearrest cooling decreased troponin I and NT-proBNP levels
after ROSC. At 240 minutes, troponin I concentration was significantly lower in the prearrest than in the Norm group (15.74 ± 2.26 vs
25.09 ± 1.85 ng/mL, P b .001), but there was no significant difference
in concentration between the Norm and post-ROSC groups (25.09 ±
1.85 vs 23.48 ± 2.66 ng/mL, P N .05). The NT-proBNP concentration
was 426 ± 23 pg/mL in the Norm group at 240 minutes after
ROSC, which was significantly higher than the concentrations of
360 ± 69 pg/mL observed in the post-ROSC group (P = .002) and
284 ± 45 pg/mL in the prearrest group (P b .002). The NT-proBNP
concentration observed in the prearrest group was significantly lower
than that of the post-ROSC group (P = .006).
3.5. Echocardiographic data
As in Table 4, at 240 minutes after ROSC, the EF and CO were lower in
the Norm group than in the other 2 groups (P b .01). End-diastolic volume of the prearrest group is bigger than that of the Norm group (P b
.01). Also, the EF and CO in the post-ROSC group were lower those in
than prearrest group (P b .05 and P b .01, respectively).
3.6. Myocardial histology
Morphologic changes were more pronounced in cells from rabbits in
the Norm group. The myocardial fibers were obviously disordered, mitochondria were severely swollen, and the cristae were vague, arranged
irregularly. In the other 2 groups, the heart morphologic structure was
much better, and myocardial fibers and mitochondrial crista structure
was clearer (Fig. 2).
4. Discussion
In this study, defibrillation was carried out before chest compression, as that is more feasible in hospitalized intensive care patients
than in those experiencing out-of hospital cardiac arrest. In the
prearrest group, ROSC occurred in 7 rabbits after the first shock and
without any chest compressions, which has not been reported in similar
studies. The mechanism by which hypothermia affects defibrillation is
not known. Buckberg et al [16] found that hypothermia during
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L. Jiang et al. / American Journal of Emergency Medicine 33 (2015) 1385–1390
Table 3
Hemodynamic data 30 to 240 minutes after achieving ROSC
30 min
HR (beats/min), mean ± SEM
Norm (n = 9)
Post-ROSC (n = 8)
Prearrest (n = 9)
MAP (mm Hg) mean ± SEM
Norm (n = 9)
Post-ROSC (n = 8)
Prearrest (n = 9)
dp/dtmax (mm Hg/s), mea ± SEM
Norm (n = 9)
Post-ROSC (n = 8)
Prearrest (n = 9)
dp/dtmin (mm Hg/s), mean ± SEM
Norm (n = 9)
Post-ROSC (n = 8)
Prearrest (n = 9)
LVEDP (mm Hg), mean ± SEM
Norm (n = 9)
Post-ROSC (n = 8)
Prearrest (n = 9)
LVESP (mm Hg), mean ± SEM
Norm (n = 9)
Post-ROSC (n = 8)
Prearrest (n = 9)
60 min
293 ± 40
208 ± 30⁎
227 ± 18⁎
289 ± 21
219 ± 16⁎
226 ± 19⁎
77 ± 16
76 ± 6
78 ± 12
79 ± 10
77 ± 6
77 ± 12
2337 ± 484
2267 ± 148
2625 ± 346
2192 ± 297
2200 ± 402
2814 ± 395⁎
2344 ± 482
1768 ± 184⁎⁎
2212 ± 534
120 min
292 ± 27
220 ± 21⁎
243 ± 21⁎
180 min
240 min
292 ± 31
230 ± 10⁎
234 ± 19⁎
289 ± 38
229 ± 17⁎
229 ± 22⁎
72 ± 10
79 ± 4
85 ± 9⁎
73 ± 11
79 ± 4
85 ± 10⁎
2177 ± 390
2193 ± 476
2814 ± 444⁎
2371 ± 507
2391 ± 383
2876 ± 351⁎⁎
2374 ± 525
2388 ± 426
2866 ± 389⁎⁎
2199 ± 372
1776 ± 352⁎⁎
2166 ± 271
2245 ± 464
1779 ± 349⁎⁎
2134 ± 327
2454 ± 345
1823 ± 413⁎
2343 ± 301
2389 ± 443
1858 ± 502⁎⁎
2368 ± 278
7.7 ± 2.8
6.9 ± 3.5
3.7 ± 3.4
5.6 ± 1.6
5.8 ± 1.6
5.4 ± 1.1
5.7 ± 1.9
4.9 ± 3.3
5.7 ± 1.6
5. 8 ± 0.9
5.7 ± 1.6
5. 3 ± 1.1
5.5 ± 1.2
5.7 ± 1.7
5.4 ± 1.1
91 ± 14
96 ± 10
105 ± 11⁎⁎
95 ± 5
94 ± 10
107 ± 9⁎
86 ± 11
96 ± 13
108 ± 13⁎
93 ± 13
100 ± 9
109 ± 10⁎
94 ± 13
100 ± 9
109 ± 11⁎
72 ± 12
75 ± 6
84 ± 11⁎⁎
⁎ P ≤ .01 vs Norm.
⁎⁎ P ≤ .05 vs Norm.
defibrillation decreased energy requirements as evidenced by reduced
oxygen consumption by the myocardium. Balaji et al [2] reported that
systemic hypothermia led to a decrease in the occurrence of arrhythmia
in patients with resistant automatic-focus tachycardias. Hypothermia
might reduce injury to myocardial cell mitochondria [17] and the cardiac sympathetic nerve activity [18] that is associated with ventricular
tachyarrhythmias [19]. A better understanding of how hypothermia affects defibrillation will help optimize CPR.
Diastolic function in prearrest group was inferior to that in the Norm
group when hypothermia was induced, but systolic function was less affected. This result is similar to previously published findings of Fischer
et al [20] and Post et al [21]. However, diastolic function in prearrest
and Norm group animals after ROSC did not differ even if the hypothermia effect it negatively, and systolic function was better in the prearrest
rabbits at that time. Hemodynamic properties were better (closer to
baseline values) in the prearrest group than in the Norm group, and cardiac function from echocardiography was the best in the 3 groups. Troponin I was significantly less elevated in the prearrest group than in the
other 2 groups. However, the histology of myocardial cells from Norm
rabbits was more disturbed than that of cells from both post-ROSC
Table 4
Echocardiographic data at baseline and at 240 minutes after the ROSC
Baseline
ROSC 4 h
EDV (mm3)
ESV (mm3)
EF
CO (mL/min)
EDV (mm3)
ESV (mm3)
EF
CO (mL/min)
Norm
Post-ROSC
Prearrest
286.98 ± 19.48
102.86 ± 7.61
0.64 ± 0.01
77.77 ± 3.63
167.43 ± 44.52
114.37 ± 34.11
0.32 ± 0.06
27.73 ± 4.80
280.77 ± 11.42
101.27 ± 5.93
0.64 ± 0.01
78.08 ± 3.79
181.35 ± 50.54
93.10 ± 28.43
0.48 ± 0.07⁎
44.17 ± 3.66⁎
266.80 ± 45.12
93.67 ± 19.03
0.65 ± 0.02
71.96 ± 10.66
252.76 ± 14.07⁎
104.80 ± 7.01
0.59 ± 0.01⁎,⁎⁎
62.93 ± 4.09⁎,⁎⁎⁎
Values are means ± SEM.
⁎ P ≤ .01 compared with Norm.
⁎⁎ P ≤ .05 compared with post-ROSC.
⁎⁎⁎ P ≤ .01 compared with post-ROSC.
and prearrest rabbits, which did not differ markedly in appearance.
Thus, no matter when hypothermia is induced, it may protect the
myocardium [22–24]. Overall, the results show that improvement in
myocardial function cannot be directly attributed to the effects of hypothermia and that some other factors may have contributed to the observed improvement in myocardial performance. First, resuscitation was
easier in the prearrest group, less defibrillation and epinephrine was
needed, and less cardiac function may have been lost. Second, because
of hypothermia, the prearrest group might have experienced less cardiac
injury after VF than the other 2 groups did. Third, delayed cooling might
have resulted in decreased protection of myocardial function.
Hypothermia was induced in this animal model before cardiac arrest; which occurs in fibrillation during hypothermic therapy or cold injury. For postcardiac arrest patients, hypothermia is widely adopted as a
protective intervention and some hypothermic patients will redevelop
VF [25]. We need more data about effect of hypothermia on defibrillation success. The American Heart Association guidelines 2010 do not
specifically state when cooling of patients should begin. Some studies
have evaluated the benefits of therapeutic hypothermia initiated during
CPR [26–28]. Some investigators have suggested that hypothermia
should be initiated as soon as possible, even intra-arrest [29,30]. Intraarrest cooling may become feasible in a clinical setting in the future
with development of rapid cooling techniques, such as liquid ventilation
of the lungs with temperature-controlled perfluorocarbons. In rabbits,
these techniques have been shown to decrease left atrial [31,22,32] or
esophageal temperature [33] to 32°C in 5 minutes. Ultrafast cooling
may become practical in humans, and in the future, maybe we would
cool down cardiac arrest patients before CPR and then resuscitate
under conditions of hypothermia in order to facilitate resuscitation.
4.1. Limitations
Some study limitations should be mentioned. First, it was not possible to blind investigators to the animals' body temperature. Second, the
mechanism of the hypothermia effect on resuscitation was not investigated. Third, the cardiac arrest model was a dysrhythmic arrest caused
by electrical shock and not caused by ischemia, which is considered as
the most common cause of death from CVD.
L. Jiang et al. / American Journal of Emergency Medicine 33 (2015) 1385–1390
1389
Fig. 2. Representative electron micrographs of subendocardial mitochondria. The myocardial fibers were obviously disordered (magnification at ×18 500, scale bar = 500 nm). A close
look at single mitochondrion of each group. Ultrastructural changes of mitochondria, including swelling and decreased cristae disintegration, were more discernible in the Norm group
and moderate in the post-ROSC group and in the prearrest group (magnification at ×23 650, scale bar = 100 nm).
5. Conclusion
Induction of hypothermia before VF led to improved cardiac function
in a rabbit VF model through improving achievement of perfusing
rhythm by first-shock defibrillation and facilitating resuscitation.
Acknowledgments
This study was supported by funding from CPR New Theory, New
Technology in Improving Cardiac Arrest Resuscitation Success
Rate (xm201313). The funders had no role in the study design, data collection, analysis, decision to publish, or the preparation of the manuscript.
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