Comparison of different inspiratory triggering settings in automated ventilators during cardiopulmonary resuscitation in a porcine model
Comparison of different inspiratory triggering settings in automated ventilators during cardiopulmonary resuscitation in a porcine model
Dingyu Tan 0 1
Jun Xu 0 1
Shihuan Shao 0 1
Yangyang Fu 0 1
Feng Sun 0 1
Yazhi Zhang 0 1
Yingying Hu 0 1
Joseph Walline 1
Huadong Zhu 0 1
Xuezhong Yu 0 1
0 Department of Emergency, Peking Union Medical College Hospital, Chinese Academy of Medical sciences , Beijing , China , 2 Division of Emergency Medicine, Department of Surgery, Saint Louis University Hospital , Saint Louis, Missouri
1 Editor: Chiara Lazzeri , Azienda Ospedaliero Universitaria Careggi , ITALY
Data Availability Statement: All relevant data are
within the paper and its Supporting Information
Funding: This work was supported by National
Health and Family Planning Commission of the
People's Republic of China (Special scientific
research funds for health industry 201502019)
(XY) and Peking Union Medical College Foundation
for Graduate Innovation (201510020101) (DT). The
funders had no role in study design, data collection
Mechanical ventilation via automated in-hospital ventilators is quite common during
cardiopulmonary resuscitation. It is not known whether different inspiratory triggering sensitivity
settings of ordinary ventilators have different effects on actual ventilation, gas exchange and
hemodynamics during resuscitation.
18 pigs enrolled in this study were anaesthetized and intubated. Continuous chest
compressions and mechanical ventilation (volume-controlled mode, 100% O2, respiratory rate 10/
min, and tidal volumes 10ml/kg) were performed after 3 minutes of ventricular fibrillation.
Group trig-4, trig-10 and trig-20 (six pigs each) were characterized by triggering sensitivities
of 4, 10 and 20 (cmH2O for pressure-triggering and L/min for flow-triggering), respectively.
Additionally, each pig in each group was mechanically ventilated using three types of
inspiratory triggering (pressure-triggering, flow-triggering and turned-off triggering) of 5 minutes
duration each, and each animal matched with one of six random assortments of the three
different triggering settings. Blood gas samples, respiratory and hemodynamic parameters
for each period were all collected and analyzed.
In each group, significantly lower actual respiratory rate, minute ventilation volume, mean
airway pressure, arterial pH, PaO2, and higher end-tidal carbon dioxide, aortic blood
pressure, coronary perfusion pressure, PaCO2 and venous oxygen saturation were observed in
the ventilation periods with a turned-off triggering setting compared to those with
pressureor flow- triggering (all P<0.05), except when compared with pressure-triggering of 20
cmH2O (respiratory rate 10.5[10/11.3]/min vs 12.5[10.8/13.3]/min, P = 0.07; coronary
and analysis, decision to publish, or preparation of
Competing interests: The authors have declared
that no competing interests exist.
perfusion pressure 30.3[24.5/31.6] mmHg vs 27.4[23.7/29] mmHg, P = 0.173; venous
oxygen saturation 46.5[32/56.8]% vs 41.5[33.5/48.5]%, P = 0.575).
Ventilation with pressure- or flow-triggering tends to induce hyperventilation and
deteriorating gas exchange and hemodynamics during CPR. A turned-off patient triggering or a
pressure-triggering of 20 cmH2O is preferred for ventilation when an ordinary inpatient hospital
ventilator is used during resuscitation.
The goal of ventilation during cardiopulmonary resuscitation (CPR) is to provide sufficient
oxygenation and removal of carbon dioxide (CO2) to improve tissue oxygenation and acidosis.
Apart from high-quality chest compressions, hyperventilation has gained increasing attention
in recent years because it may negatively affect outcomes in cardiac arrest [1±3]. Manual
ventilation with respiratory rates greater than 20 breaths/ min is common during CPR from cardiac
arrest [4±6]. An automated transport ventilator (ATV) was found to be as effective as a bag
valve mask to deliver ventilation during CPR once the airway is secured [
], and it is
recommend by the current guidelines for prolonged resuscitation . In addition, using of ATV may
help to avoid uncontrolled ventilation and improve the quality of chest compressions [
However, mechanical ventilation by an ordinary automated ventilator rather than an ATV is quite common during resuscitation in actually clinical practice especially in inpatient hospital settings.
Different from the totally time-triggered mandatory breaths of Intermittent Positive Pres
sure Ventilation (IPPV) in ATV, the IPPV mode in most hospital-based ventilators (such as
volume controlled mode) works with time- and patient-triggering simultaneously in order to
increase the patient-ventilator synchrony [
]. Patient triggering systems such as
pressureand flow-triggering cannot be turned off in most of the commonly used modern ventilators.
Except for respiratory rate (RR), using other ventilatory parameters (e.g. minute ventilation,
peak pressure limit) during advanced life support is not recommend under current guidelines
]. We observed in clinical practice that the changes in airway pressure and airflow induced
by chest compressions during CPR may lead to abnormal inspiratory triggering and cause
remarkably high ventilation rates. The effects of different inspiratory triggering sensitivity
settings of ventilators on actual ventilation during CPR was seldom reported. Additionally, we
wanted to see if no triggering was of any benefit in comparison to pressure- or flow- triggering.
In this study we investigated the influence of different inspiratory triggering settings using typical hospital-based ventilators on actual ventilation, gas exchange and hemodynamics in a porcine model of cardiac arrest.
Materials and methods
With approval of the ethics committee for animal experiments at Peking Union Medical Col
lege Hospital, the study was performed on a total of 18 domestic pigs (weight, 31.1±1.8 kg).
The animals were fasted overnight and premedicated with one dose of intramuscular pentobarbital sodium (30 mg/kg), diazepam (0.3 mg/kg) and atropine (0.02 mg/kg). The animals
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were then placed supine in a U-shaped fixing frame. An intravenous catheter was inserted into
a lateral ear vein and followed by propofol infusion (2±3 mg/kg/hr) to maintain anesthesia.
Each pig was intubated with a size 6.5 endotracheal tube and then mechanically ventilated
with room air, using volume-control mode (Hamilton-G5, Hamilton Medical AG; Bonaduz,
Switzerland), with a tidal volume of 10 mL/kg and a RR adjusted to maintain partial pressure
of end-tidal carbon dioxide (PETCO2) at 35~40 mmHg and pulse oxygen saturation > 95%.
Arterial blood gases (Gem 3000; Instrumentation Laboratory, Bedford, MA) were analyzed to
verify the baseline conditions. A warming blanket was used to maintain the animal's
temperature between 36±38ÊC.
The right internal jugular vein and left common carotid artery were surgically exposed and
cannulated for right atrial pressure (RAP) and central aortic blood pressure (AoP)
measurements, as well as blood sampling. The left external jugular vein was also fitted with a catheter
which provided access for ventricular fibrillation induction. Normal saline solution at 5ml/kg/
hr was infused prior to the induction of ventricular fibrillation to maintain RAP between 3
and 5 mm Hg. Electrocardiograms, AoP and RAP were continuously monitored and recorded
by a T8 Mindray monitor (Mindray Biological Medical Electronic Co, Ltd, Shenzhen, China).
Coronary perfusion pressure (CPP) was calculated as the gradient between AoP and RAP during the decompression phase of chest compressions. RR, minute ventilation volume and airway pressure were continuously recorded by a BIOPAC MP-150 system via a piezometric tube and a flow sensor linked to the endotracheal tube.
Ventricular fibrillation was induced by 24V/50Hz AC current with a right ventricular internal
pacing electrode. After 3 minutes of untreated ventricular fibrillation without any ventilation,
continuous chest compressions via a mechanical CPR device (WISH-SL-FS-A, Wuhan,
China) were started at a rate of 100 compressions/min and a depth of 30% of the
anteroposterior chest diameter. Mechanical ventilation (Hamilton-G5) was performed simultaneously for
three periods of 5 minutes each, using a volume-controlled mode with a constant flow of 30L/
min, zero end-expiratory pressure, FiO2 1.0, RR 10/min, tidal volume of 10 mL/kg, I:E 1:2, and
the upper airway pressure limit was set to 60 cmH2O (Fig 1). According to the different
inspiratory triggering sensitivity settings, the animals were divided into three groups. In the first
group of six pigs (Group trig-4), three periods (5 minutes each) of mechanical ventilation were
characterized by a pressure-triggering sensitivity of 4 cmH2O, a flow-triggering sensitivity of 4
L/min, and turned-off triggering respectively. Similar to Group trig-4, six pigs in Group
trig10 were ventilated with a pressure-triggering of 10 cmH2O, a flow-triggering of 10 L/min and
turned-off triggering, while six pigs in Group trig-20 were ventilated with a pressure-triggering
of 20 cmH2O, a flow-triggering of 20 L/min and turned-off triggering. Six sequences in each
group were generated due to random assortment of the three different triggering settings, and
each animal in each group was ventilated in accordance with one of the six sequences. Arterial
and central venous blood gas samples were drawn at baseline and at the endpoint of each 5
minute ventilation period. The animals were finally sacrificed by infusion of potassium
chloride at the end of the experiment. Respiratory and hemodynamic parameters at last minute of
each period were collected, and the mean values were analyzed.
No.1 Turned-off - - - - Pressure-triggering - - - - Flow-triggering
No.2 Turned-off - - - - Flow-triggering - - - - Pressure-triggering
No.3 Pressure-triggering - - - - Turned-off - - - - Flow-triggering
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Fig 1. Experimental protocol. VF, ventricular fibrillation.
No.4 Pressure-triggering - - - - Flow-triggering - - - - Turned-off
No.5 Flow-triggering - - - - Turned-off - - - - Pressure-triggering
No.6 Flow-triggering - - - - Pressure-triggering - - - - Turned-off
Non-parametric tests were applied in this study due to the small sample size. Statistical analysis
was performed with SPSS 17.0 for Windows (SPSS, Inc.), using the Mann-Whitney U test or
Kruskal-Wallis H test. Continuous variables are expressed as median (25th/75th percentiles)
except the animals' weight. Statistical significance was fixed at a P value of less than 0.05.
Data from all 18 animals were included in the analysis. The results of respiratory parameters, hemodynamic parameters, and blood gases analyses were similar in the three groups at baseline (Table 1).
In each group, turned-off triggering provided a RR identical to the set value, while the pres
sure- and flow-triggering could induce significantly higher actual RR with the exception of a
pressure-trigger of 20 cmH2O (all P<0.05, Table 2). Except for the pressure-trigger of 20
cmH2O, significantly higher minute ventilation volumes, mean airway pressures, and lower
PETCO2, AoP and CPP were also induced by the pressure- and flow-triggering settings
compared to turned-off triggering (all P<0.05, Fig 2).
In each group, significantly lower arterial pH, PaO2, and higher PaCO2 were observed in
the periods with turned-off triggering compared to those with pressure- or flow- triggering (all
P<0.05), except in the comparison with pressure triggering in Group trig-20 (Table 3). The
venous blood gas analyses showed that most of the differences of venous pH, PvO2 and PvCO2
between the different triggering settings were not statistically significant. Turned-off triggering
was related to higher venous oxygen saturation (SvO2) than those of pressure- or flow-
triggering settings in each group (all P<0.05), with the exception of a pressure-triggering of 20
cmH2O (46.5[32/56.8] % vs 41.5[33.5/48.5] %, P = 0.575).
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RR, Respiratory rate; MV, Minute ventilation volume; AwP, Mean airway pressure; PETCO2, Partial pressure of end-tidal carbon dioxide; AoP, Aortic blood
pressure; RAP, Right atrial pressure; CPP, Coronary perfusion pressure; SvO2, Venous oxygen saturation.
In Group trig-20, the venous-arterial CO2 gradients for turned-off triggering,
pressure-triggering and flow-triggering were 8(-0.25/10) mmHg, 15(2.5/26) mmHg and 31.5(29.8/35.3)
mmHg respectively (Fig 3). The venous-arterial CO2 gradients for flow-triggering were
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Fig 2. Aortic blood pressure, right atrial pressure and mean airway pressure during the inspiratory phase of an animal in Group trig-20. The
period indicated by dotted box is the decompression phase of chest compressions. Coronary perfusion (shadow area) is indicated by the area
between red and blue line in the dotted box. (A), Turned-off triggering. (B), A pressure-triggering of 20 cmH2O. (C), A flow-triggering of 20 L/min.
significantly higher than those of turned-off triggering (P = 0.006). The comparison between
turned-off triggering and pressure-triggering did not show statistical significance (P = 0.148).
This study investigated ventilation via a typical hospital ventilator using different inspiratory
triggering settings during CPR. Compared to the turned-off patient triggering, most settings of
pressure- or flow-triggering induced hyperventilation through a high RR, with the exception
of pressure-triggering at 20 cmH2O. Though a higher PaO2 was observed, elevated mean
airway pressures and deteriorating CPP, PETCO2 and SvO2 seen with these settings indicated
adverse prognoses. A pressure-triggering of 20 cmH2O had similar ventilation volume, gas
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Fig 3. Venous-arterial CO2 gradients in Group trig-20 (median, 25/75% percentiles, min/max) [mmHg].
exchange and hemodynamics as compared to turned-off triggering, and could be an
alternative choice if an ATV or turned-off patient triggering was not available in clinical practice.
Excessive ventilation is strongly suggested to be avoided in the current guidelines, due to its
adverse effects increasing intrathoracic pressure, decreasing venous return, coronary
perfusion, and diminishing cardiac output and survival [
]. Avoidance of hyperventilation
during CPR is a broad consensus, though clinical studies confirming the association between
hyperventilation and cardiac arrest outcomes are limited. However, hyperventilation
commonly occurs during CPR with RR exceeding 10 breaths/min 63% of the time and exceeding
20 breaths/min 20% of the time, despite guideline recommendations . The precipitating
factors of hyperventilation are usually multifactorial including an adrenaline-driven arousal
response, resuscitator inexperience, and CPR delivered at off-hours [
6, 14, 15
]. RR by manual
ventilation could even reach 37 breaths/min with advanced airways, and providers often fail to
ventilate at recommended rates even after retraining [
1, 4, 16
The use of a mechanical ventilator during CPR can theoretically eliminate hyperventilation
by totally controlling ventilation rates and tidal volumes without patient triggering. An ATV is
recommended in the guidelines as one of the ventilation alternatives for prolonged
resuscitation efforts to provide adequate ventilation and allow resuscitators to perform other tasks [
while the automatic mode of the oxygen-powered, flow-limited ventilator should not be used
due to its adverse effects on venous return and forward blood flow [
]. The mechanical
properties of typical hospital-based ventilators are usually superior to transport ventilators, and
these ordinary ventilators are often involved in CPR due to their availability and convenience
in our clinical practice. However, patient-triggering cannot be turned off in most modern
ventilators (e.g. Puritan Bennette 7200ae & 840, MAQUET servo-i, Drager infinity C500, and GE
Engstrom carestation, among others). The current guidelines do not give any specific ventilatory recommendations except for the RR with a secured airway, and, to the best of our knowledge, there are no studies focusing on different inspiratory triggering settings during CPR until now.
In general, the maximum adjustable range of pressure- or flow-triggering of most modern
ventilators is 20 cmH2O or L/min. This study demonstrated that a pressure-triggering of 20
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cmH2O rather than a flow-triggering of 20 L/min could effectively control hyperventilation.
Because of design characteristics, flow-triggering provides more sensitive triggering and
relatively shorter time delay than pressure-triggering [
]. It's reasonable to surmise from our
study that airway pressures are usually between -10 and -20 cmH2O, while airflow is more
than 20 L/min in most cases during the decompression phase of chest compressions. Adverse
effects of hyperventilation were verified in this fundamental research again. High ventilation
rates greater than 20 breaths/min induced high minute ventilation volume, increased mean
airway pressure, and decreased CPP in this study.
However, contradictory viewpoints and research challenging the adverse effects of
hyperventilation or high airway pressures during CPR have emerged in recent years [20±22]. Higher
mean airway pressure was found to be associated with higher ROSC in clinical settings [
novel ventilation mode (Chest Compression Synchronized Ventilation, CCSV) which
increases cyclic intrathoracic pressure differences and avoids negative airway pressure shows
better effects on oxygenation and hemodynamics compared to IPPV [
]. Meanwhile, the
need for artificial ventilation in the first minutes of CPR has also been challenged in the past
several years [
]. Passive ventilation such as continuous positive airway pressure (CPAP) with
pure oxygen via a Boussignac device or CPAP plus pressure support ventilation, was found to
an effective alternative to mechanical ventilation with similar or superior gas exchange [
]. Nevertheless, positive-pressure ventilation is still the ªgold standardº of ventilation during
CPR, though further investigations are needed to clarify the specific effects of ventilation vol
ume and airway pressure on the outcomes of CPR.
As regards gas exchange in this study, high RR caused by pressure- and flow-triggering
were correlated with decreased PETCO2, alkalosis and better arterial oxygenation. Arterial
blood gas values were often used as measurable indicators of resuscitation effects in may
studies of CPR [27±29]. However, PaCO2 and PaO2 are simultaneously influenced by ventilation
and pulmonary blood flow [
]. With significantly decreasing pulmonary blood flow
(increasing ventilation/perfusion ratio), PaO2 increases and PaCO2 decreases, approaching the
composition of inspired gas, which is opposite to conventional practice [
]. Similar to the current
study, increased PaO2 and decreased PaCO2 during low blood flow states of CPR, may indicate
not only adequate or excessive ventilation but also the negative effects of deteriorating blood
flow. In general, oxygen delivery to the heart and brain is limited by blood flow rather than by
arterial oxygen content during CPR [
9, 31, 32
Venous blood gases are thought to be more useful than arterial blood gases to assess perfu
sion during resuscitation, because they are less affected by ventilation changes [
Actually, similar values of venous blood gases analysis were observed in most groups in our study,
except that controlled ventilation rates with turned-off triggering or pressure-triggering of 20
cmH2O showed better SvO2. However, the same phenomenon was also observed in human
CPR . Subjects with restoration of spontaneous circulation (ROSC) demonstrated signifi
cantly different values of venous PH, PO2, and PCO2 during resuscitation, while a higher SvO2
indicated high rate of ROSC from cardiac arrest.
In addition to decreased CPP and SvO2, flow-triggering also correlated with increased
venous-arterial CO2 gradients. Low blood flow states such as during chest compressions or
shock, PaCO2 positively correlates with blood flow while venous PCO2 negatively correlates
with blood flow [
]. The increased venous-arterial CO2 gradients in this study indicated
decreased blood flow during CPR, and suggest again that hyperventilation due to
flow-triggering deteriorates cardiac output and tissue blood flow.
Our study has several limitations. First, the sample of animals was relatively small and outcomes of resuscitation efforts such as ROSC could not be detected and compared because of the cross-over design. Second, 5 minutes for each ventilation period was relatively short. That
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was chosen because the differences of respiratory parameters, gas exchange and
hemodynamics between different triggering settings were significant after a ventilation duration of 5
minutes, and prolonged CPR would induce rapid deterioration of artificial circulation. Finally, an
ATV was not involved in our study to serve as a point of comparison with our hospital-based
ventilators. When the triggering of a ventilator is turned off, its ventilation process is basically
identical to that of an ATV. Furthermore, the purpose of this study was to evaluate the
feasibility of using different inspiratory triggering settings in an ordinary ventilator during CPR.
In conclusion, for ordinary automated ventilators found in inpatient hospital settings, pres
sure-triggering of 4 or 10 cmH2O and flow-triggering are improper for ventilation during
CPR, due to their induction of hyperventilation leading to the deterioration in gas exchange
and hemodynamics. Turned-off patient triggering is preferred, and a pressure-triggering of 20
cmH2O could be a viable alternative if turned-off triggering is not available.
S1 File. Relevant data underlying the findings described in manuscript.
We thank the Institute of Life Monitoring, Mindray Corporation for providing the T8 monitors used in this study. Mindray Corporation did not have any role in the study design, data collection, data analysis, preparation of the manuscript, or decision to publish.
Conceptualization: HZ XY DT JX JW.
Formal analysis: DT JX SS FS YH YZ.
Funding acquisition: XY DT.
Investigation: DT SS YF FS YH YZ.
Methodology: DT JX SS YF.
Project administration: XY HZ.
Resources: XY DT JX HZ JW.
Writing ± original draft: DT JX SS HZ XY.
Writing ± review & editing: DT JX SS HZ XY JW.
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