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Cardiology in the Young
cambridge.org/cty
Original Article
Cite this article: Stromberg D, Carvalho K,
Marsden A, Mery CM, Immanuel C, Mizrahi M,
and Yang W (2021). Standard CPR versus
interposed abdominal compression CPR in
shunted single ventricle patients: comparison
using a lumped parameter mathematical
model. Cardiology in the Young, page 1 of 7.
doi: 10.1017/S1047951121003917
Received: 30 January 2021
Revised: 21 July 2021
Accepted: 28 August 2021
Keywords:
IAC-CPR; single-ventricle; interposed
abdominal compressions
Author for correspondence:
D. Stromberg, MD, Dell Children’s Medical
Center, 4900 Mueller Ave., Austin, TX 78723,
USA. Tel: (214) 533-5348; Fax: 512-380-7532.
E-mail: dstromberg@austin.utexas.edu
© The Author(s), 2021. Published by Cambridge
University Press.
Standard CPR versus interposed abdominal
compression CPR in shunted single ventricle
patients: comparison using a lumped parameter
mathematical model
Daniel Stromberg1, Karen Carvalho1, Alison Marsden2
,
3, Carlos M. Mery1,
Camille Immanuel1, Michelle Mizrahi1and Weiguang Yang2
,
3
1Departments of Pediatrics and Surgery and Perioperative Care, Texas Center for Pediatric and Congenital Heart
Disease, UT Health Austin/Dell Children’s Medical Center, Austin, TX, USA; 2Department of Pediatrics, Stanford
University, Stanford, CA, USA and 3Department of Bioengineering, Stanford University, Stanford, CA, USA
Abstract
Introduction: Cardiopulmonary resuscitation (CPR) in the shunted single-ventricle population
is associated with poor outcomes. Interposed abdominal compression-cardiopulmonary resus-
citation, or IAC-CPR, is an adjunct to standard CPR in which pressure is applied to the abdo-
men during the recoil phase of chest compressions. Methods: A lumped parameter model that
represents heart chambers and blood vessels as resistors and capacitors was used to simulate
blood flow in both Blalock-Taussig-Thomas and Sano circulations. For standard CPR, a pre-
scribed external pressure waveform was applied to the heart chambers and great vessels to sim-
ulate chest compressions. IAC-CPR was modelled by adding phasic compression pressure to
the abdominal aorta. Differential equations for the model were solved by a Runge-Kutta
method. Results: In the Blalock-Taussig-Thomas model, mean pulmonary blood flow during
IAC-CPR was 30% higher than during standard CPR; cardiac output increased 21%, diastolic
blood pressure 16%, systolic blood pressure 8%, coronary perfusion pressure 17%, and coronary
blood flow 17%. In the Sano model, pulmonary blood flow during IAC-CPR increased 150%,
whereas cardiac output was improved by 13%, diastolic blood pressure 18%, systolic blood pres-
sure 8%, coronary perfusion pressure 15%, and coronary blood flow 14%. Conclusions: In this
model, IAC-CPR confers significant advantage over standard CPR with respect to pulmonary
blood flow, cardiac output, blood pressure, coronary perfusion pressure, and coronary blood
flow. These results support the notion that single-ventricle paediatric patients may benefit from
adjunctive resuscitation techniques, and underscores the need for an in-vivo trial of IAC-CPR
in children.
The immediate goals of CPR for children experiencing an arrest are to deliver nutrient oxygen to
peripheral vascular beds and reestablish spontaneous circulation. Since standard CPR provides
only a limited percentage of normal cardiac output (approximately 15–30%),1,2blood flow to
vital organs is severely compromised during prolonged resuscitation. As a result, increased
duration of CPR has been associated with poor outcome.3–7Furthermore, the ability to achieve
adequate “diastolic”blood pressures during the relaxation phase of thoracic compressions has
been shown to be associated with outcome.8,9In adults, those who do not generate >16 mmHg
diastolic blood pressure during resuscitation do not experience return of spontaneous circula-
tion presumably due to poor coronary perfusion pressure.10 In children, Berg et al showed that a
threshold diastolic blood pressure of 25 mmHg in those <1 year of age, and 30 mmHg in those
>1 year of age, increased the probability of achieving return of spontaneous circulation.11
Standard approaches to elevate diastolic blood pressure during resuscitation include changing
the force or location of compressions, allowance of full chest recoil, volume administration, and
catecholamine/vasopressor administration. However, these treatments may have their own
respective consequences such as heart distension (with worsened atrio-ventricular valve regur-
gitation and pulmonary oedema), and increased myocardial oxygen consumption. Thus, they
may further strain the heart at a time when functional reserve is low and cardiac recovery is
needed.
IAC-CPR is a technique in which force is applied to the abdomen during the recoil phase of
chest compressions. It includes all elements of standard cardiopulmonary resuscitation, thereby
serving as an adjunct to traditional resuscitation. IAC-CPR works by external force transmission
through the abdomen to the aorta. This leads to an increase in aortic diastolic pressure and
enhanced retrograde flow to the coronary arteries and prograde flow to the brain in a manner
similar to intra-aortic balloon counterpulsation or external counterpulsation.12 It also results in
hydrostatic compression of intra-abdominal veins, which advances blood into the thoracic
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compartment during the relaxation phase of chest compressions.
This refilling of the intrathoracic blood pool improves cardiac
output with subsequent chest compressions. Finally, IAC-CPR
augmentation of baseline venous pressure coupled with mainte-
nance of an adequate arteriovenous gradient overcomes capillary
closing pressure and thereby improves vital organ perfusion.13
IAC-CPR has been evaluated in both animals and adult
humans. In a canine resuscitation model of electrically induced
ventricular fibrillation, IAC-CPR was found to increase oxygen
delivery, arterial systolic and diastolic blood pressure, and cardiac
output compared to standard CPR.14 IAC-CPR has also been
shown to augment carotid arterial flow in dogs by direct intravas-
cular measurement. Blood flow averaged 22.8% of control values
during IAC-CPR versus 8.7% during standard cardiopulmonary
resuscitation.15 More recently, these data were corroborated in a
swine ventricular fibrillation model. Animals receiving IAC-CPR
as opposed to standard CPR during arrest demonstrated greater
systolic and diastolic blood pressure, coronary perfusion pressure,
and end-tidal CO
2
(as a surrogate measure of cardiac output).
Return of spontaneous circulation was greater in the IAC-CPR
cohort, and neurologic examinations in survivors who received
IAC-CPR were superior to those who underwent standard CPR.16
Human studies of IAC-CPR have yielded similar benefits. Data
from four randomized clinical trials of IAC-CPR have shown
improved resuscitation rates and survival for adult patients experi-
encing in-hospital cardiac arrest.17 Formal meta-analysis of all
clinical trials of IAC-CPR versus standard CPR revealed improve-
ment in the rate of return of spontaneous circulation by 10.7%
(p =0.006), and a trend toward increased hospital discharge with
intact neurologic function of 8.7% (p =0.06). When meta-analysis
was limited to in-hospital trials (n =279), return of spontaneous
circulation was 52% with IAC-CPR versus 26% with standard
cardiopulmonary resuscitation (p <0.0001). This suggests that
only 4 patients would need to be treated with IAC-CPR to achieve
return of spontaneous circulation in one additional patient.18
IAC-CPR has been recommended as an acceptable alternative
to standard CPR for adult in-hospital resuscitation (Class IIb rec-
ommendation per the American Heart Association guidelines).19
However, no experimental data on which to make paediatric
recommendations, either for or against IAC-CPR, yet exist. Our
interest in IAC-CPR arose from our clinical observation that chil-
dren with palliated single ventricle lesions and shunt-dependent
pulmonary blood flow are extremely difficult to resuscitate with
good outcomes owing to their severe hypoxemia during CPR;
and our concern that increased intrathoracic pressure transmitted
to the lungs during standard CPR may limit pulmonary blood flow
and reduce efficacy of resuscitative efforts. Thus, we postulated that
IAC-CPR might provide a novel mechanism for counteracting the
problem of pulmonary blood flow limitation during single ven-
tricle resuscitation by increasing blood pressure during CPR “dias-
tole,”and directly enhancing retrograde (in Blalock-Taussig-
Thomas) or prograde (in Sano) shunt perfusion. Furthermore,
we hypothesised that the increase in pulmonary blood flow during
IAC-CPR would not diminish cardiac output compared to stan-
dard CPR via a steal phenomenon. Rather, IAC-CPR would
increase overall cardiac output in addition to pulmonary blood
flow through augmentation of venous return.
Materials and methods
We employed a previously described lumped parameter model
wherein heart chambers and blood vessels are represented as a
series of resistor and capacitor circuits to simulate blood flow.20
The lumped parameter model was modified to represent single
ventricle circulation with either a Blalock-Taussig-Thomas or
Sano shunt (Fig 1). By making an analogy between blood flow
and electrical current in which pressure drop is analogous to volt-
age, and flow rate is analogous to current, flow Qthrough a vessel
was determined by Ohm’s law (Q=P/R), where Pis the pressure
drop across the vessel and Ris the resistance. For a capacitor that
represents vessel compliance, the flow–pressure relationship was
given by dP/dt =Q/C, where Cis the capacitance (Fig 2a).
When an external force is applied to the capacitor chamber, we
defined dP/dt =Q/Cþ(dP_chest)/dt, where P
chest
is the compres-
sion pressure; the same reasoning was applied to abdominal com-
pression using P
abd
during IAC-CPR (Fig 2b). To model the aortic,
atrioventricular, and internal jugular valves, unidirectional flow
was allowed for R_Out,R_LA and R_SVC. By applying these pres-
sure-flow equations to each component in the lumped parameter
model, we derived an ordinary differential equation system that
was solved numerically by a standard explicit fourth order
Runge-Kutta method. Since initial pressures and flow in the
lumped parameter model were set to zero, and variations between
cycles due to the transient response of resistors and capacitors
existed before a stable state was achieved, we simulated 15 cycles
to obtain periodic results and used the last five cycles to calculate
the quantities of interest. Time integration step size was set to
0.00075 second to avoid numerical oscillations caused by a large
step size.
Assumed values for haemodynamic parameters are listed in
Table 1. These were modelled after haemodynamic catheterisation
data of single ventricle patients from within our institution in the
last 2 years, and from published data.20 For all forms of CPR, a
chest compression rate of 100 was employed per American
Heart Association Pediatric Advanced Life Support Guidelines.21
External pressures (max 80 mmHg) were applied to the heart
chambers and great vessels. One hundred percent force transmis-
sion was applied to the single ventricle, whereas 80% was applied
to the pulmonary arteries to simulate a gradient for forward
flow. IAC-CPR was modelled in both types of single ventricle
palliations by adding additional phasic compression pressures
(max 60 mmHg) to the abdominal aorta. A duty cycle of 50%
was employed with half-sinusoidal functions (Fig 3).20
Hemodynamic values are expressed as means, and percent
differences between them.
Results
In the Blalock-Taussig-Thomas shunt model, pulmonary blood
flow during IAC-CPR was 30% higher than pulmonary blood flow
during standard CPR (0.92 versus 0.71 L/minute). Moreover, this
did not occur at the expense of systemic cardiac output, as cardiac
output in IAC-CPR was increased by 21% (1.75 versus 1.45 L/
minute). Diastolic blood pressure was also higher during IAC-
CPR (16% increase, 36 versus 31 mmHg, Fig 4), as were coronary
perfusion pressure (17% increase, 27 versus 23 mmHg, Fig 5) and
coronary blood flow (17% increase, 0.14 versus 0.12 L/minute).
Systolic blood pressure was improved by IAC-CPR, though only
by 8% (84 versus 78 mmHg).
In the Sano model, pulmonary blood flow during IAC-CPR
more than doubled compared to standard CPR (0.1 versus
0.04 L/minute). However, Sano pulmonary blood flow was consid-
erably lower during both forms of CPR compared to the Blalock-
Taussig-Thomas shunt condition due to a greater assumed shunt
2 D. Stromberg et al.
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resistance, and a reduced pressure gradient from the single ven-
tricle to the pulmonary arteries. Cardiac output was improved
in IAC-CPR by 13% (0.94 versus 0.83 L/minute), as were diastolic
blood pressure (18% increase, 39 versus 33 mmHg, Fig 6), systolic
blood pressure (8% increase, 86 versus 80 mmHg), coronary per-
fusion pressure (15% increase, 31 versus 27 mmHg, Fig 7), and
coronary blood flow (14% increase, 0.16 versus 0.14 L/minute).
Discussion
IAC-CPR has been shown to increase “diastolic”blood pressure
during the relaxation phase of chest compressions, thereby
enhancing retrograde coronary perfusion and prograde cerebral
blood flow.14,22 In theory, this diastolic blood pressure elevation
should also augment flow through any shunt capable of producing
aortic run-off, such as an aorto-pulmonary, or Blalock-Taussig-
Thomas shunt. However, this phenomenon has never been studied
during CPR nor scientifically demonstrated. Our investigation,
using a single ventricle mathematical model, has demonstrated
that IAC-CPR may augment Blalock-Taussig-Thomas shunt flow,
and thus, pulmonary blood flow (by 26%) compared to standard
cardiopulmonary resuscitation. In addition, our construct suggests
that IAC-CPR increases both pulmonary blood flow and cardiac
output (by 20%) compared to standard cardiopulmonary resusci-
tation, thereby avoiding a detrimental scenario in which the tech-
nique diminishes much-needed systemic output by preferentially
routing blood to the lungs.
In a similar manner, IAC-CPR in the Sano model increased pul-
monary blood flow and cardiac output by 100 and 15%, respectively,
compared to standard cardiopulmonary resuscitation. However, Sano
Figure 1. Schematic of single ventricle blood vessels and heart chambers represented as a series of resistor and capacitor circuits. (a) BTT shunt with connection between the
aorta (C-AAo) and pulmonary arteries (C-Pul). (b) Sano shunt showing connection between the single ventricle (C-SV) and the pulmonary arteries (C-Pul). Capacitors: C-
AAo =ascending aorta, C-Dao =descending aorta, C-IVC =inferior vena cava, C-RA =right atrium, C-LA =left atrium, C-Pul =pulmonary arteries, C-SV =single ventricle, C-
Car =upper body arteries, C-SVC =upper body vessels/superior vena cava. Resistors: R-AAo =ascending aorta, R-Upper =upper body vessels, R-SVC =superior vena cava,
R-RA =atrial septum, R-LA =atrio-ventricular valve, R-Out =neo-aorta, R-Sano =Sano shunt, R-BTTS =BTT shunt, R-Pul =pulmonary vessels, R-CArt =coronary vessels, R-
Dao =descending aorta, R-Lower =lower body vessels, R-IVC =inferior vena cava. BTT =Blalock-Taussig-Thomas.
Cardiology in the Young 3
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Figure 2. (a) Modifications of Ohm’s Law for resistors and capacitors in the lumped
parameter model applied to single ventricle physiology. (b) Definitions of dP/dt rela-
tive to chest or abdominal compression. Key: Q =flow, P =pressure, R =resistance,
dP/dt =change in pressure over time. P
chest
=pressure of chest compression,
P
abd
=pressure of abdominal compression.
Table 1. Input values for lumped parameter model
Parameter Assumed value
R-Out 7 mmHg/L/second
R-RA 20 mmHg/L/second
R-AAo 150 mmHg/L/second
R-Upper 12,100 mmHg/L/second
R-SVC 110 mmHg/L/second
R-DAo 88 mmHg/L/second
R-IVC 88 mmHg/L/second
R-Lower 3300 mmHg/L/second
R-CArt 11,400 mmHg/L/second
R-BTTS 1320 mmHg/L/second
R-Sano 3750 mmHg/L/second
R-Pul 600 mmHg/L/second
R-LA 50 mmHg/L/sec ond
C-AAo 0.000936 L/mmHg
C-SV 0.012 L/mmHg
C-RA 0.0145 L/mmHg
C-DAo 0.000468 L/mmHg
C-IVC 0.0234 L/mmHg
C-Car 0.000156 L/mmHg
C-SVC 0.001 L/mmHg
C-Pul 0.01 L/mmHg
C-LA 0.0128 L/mmHg
P
max chest
80 mmHg
P
max abd
60 mmHg
Compression fraction in each cycle 0.5
Figure 3. External compressing pressures in chest and abdominal compression
cycles. Note the 50% duty cycle, the 80 mmHg max chest pressure, and the
60 mmHg max abdominal pressure.
Figure 4. Blalock-Taussig-Thomas shunt haemodynamics showing a highe r diastolic
blood pressure during IAC-CPR.
Figure 5. Coronary perfusion pressure during IAC-CPR in the Blalock-Taussig-
Thomas shunt haemodynamics.
Figure 6. Sano shunt haemodynamics also showing a higher diastolic bloodpressure
during IAC-CPR.
4 D. Stromberg et al.
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shunt flow was significantly lower than that of the Blalock-Taussig-
Thomas shunt. The lower pulmonary blood flow calculated for the
Sano model was not surprising given that Sano pulmonary blood flow
is dependent upon the gradient between the right ventricle and pul-
monary arteries at all points in the resuscitation cycle. This gradient is
modest during chest compressions due to raised intrathoracic pres-
sure in cardiopulmonary resuscitation systole, while during cardio-
pulmonary resuscitation diastole there is no aortic driving pressure
to improve pulmonary perfusion as there is with a Blalock-
Taussig-Thomas shunt.
The cardiac output in our model was determined by the pres-
sure gradient between the ventricle and the ascending aorta (C-SV
and C-AAO, Fig 1) since the resistance R-out was kept unchanged.
Thus, in the presence of a Blalock-Taussig-Thomas shunt which
increases cross-sectional area for flow and aortic runoff, the pres-
sure gradient (and cardiac output) is increased. In contrast, the
ventricular-aortic pressure gradient with the higher resistance
Sano shunt is smaller, resulting in a lower calculated cardiac out-
put. In both single ventricle palliation types, an increase in cardiac
output was seen during IAC-CPR. This is concordant with a recent
adult trial in which IAC-CPR increased end-tidal CO
2
, a surrogate
measure of cardiac output, by 38% versus standard CPR.23
The 19% increase in diastolic blood pressure demonstrated during
IAC-CPR improved hemodynamic profiles –there was an increase in
coronary perfusion pressure (13%) and coronary blood flow (17%) in
the Blalock-Taussig-Thomas shunt model, and in the Sano model
(coronary perfusion pressure increased 19%, coronary blood flow
increased 14%). These virtual findings are consistent with the known
physiologic effects of IAC-CPR seen in animal studies and human tri-
als of the resuscitation technique.22,24,25 For example, in a recent swine
ventricular fibrillation model, coronary perfusion pressure was
increased by 19%; other animal models have demonstrated two-fold
coronary perfusion pressure elevations, while human measurements
have shown more modest improvements.24–27 Similarly, in a ventricu-
lar fibrillation canine resuscitation model using microspheres, coro-
nary blood flow was improved by 22.7% with IAC-CPR.28 These
correlations imply that our model may accurately reflect hemo-
dynamic conditions during CPR. Accordingly, our results may por-
tend better outcomes for single ventricle patients who undergo
IAC-CPR versus standard CPR.
While it is known that outcomes from single ventricle resusci-
tation with conventional CPR are poor, the influence of shunt type
remains unclear. Single ventricle children have a higher rate of
arrest, likely due to increased myocardial work demand on the sin-
gle ventricle from volume overload, imbalances in Qp:Qs, and
shunt occlusions. They also have a greater chance of demise from
an arrest, and an increased need for rescue extracorporeal
membrane oxygenation.29 Lowry et al, using an administrative
inpatient database, demonstrated that single ventricle patients
have five-fold increased odds of cardiac arrest compared to chil-
dren with a biventricular circulation. Furthermore, single ventricle
patients exhibit decreased survival after CPR (mortality OR 1.7),
even after adjustment for covariates.29 Alten et al, using
Pediatric Cardiac Critical Care Consortium data, documented
an arrest rate in single ventricle patients near 16%, with survival
that was only half that of cardiac arrest in other surgical catego-
ries.30 Extracorporeal cardiopulmonary resuscitation, utilised for
failure to achieve return of spontaneous circulation after an arrest,
is also common, occurring in 13–20% of stage one postoperative
patients. Risk factors for extracorporeal membrane oxygenation
include low birth weight, longer cardiopulmonary bypass time,
small ascending aorta (<2 mm), mitral stenosis with aortic atresia,
intraoperative shunt revision, and a Sano RV-PA shunt type.31
This suggests that Sano patients may have a less favourable
response to CPR (thus necessitating extracorporeal cardiopulmo-
nary resuscitation), a fact which may be corroborated by recent
examination of the PICqCPR arrest cohort wherein survival to
hospital discharge was much better among Blalock-Taussig-
Thomas shunt patients than Sano patients (89% versus 38%,
p<0.05).32 If our model is accurate with regard to the level of car-
diac output achieved during resuscitation of Blalock-Taussig-
Thomas shunt versus Sano palliation patients, one could speculate
that the lower Sano cardiac output explains the outcome difference.
It is also conceivable that single ventricle resuscitation outcomes
are poor, and particularly those in Sano (vs Blalock-Taussig-
Thomas shunt) patients, due to determinants of pulmonary blood
flow. Chest compressions raise intrathoracic pressure and reduce pul-
monary blood flow in both Sano and Blalock-Taussig-Thomas
shunted patients.33 This results in systemic blood flow with low oxy-
gen content, which in the presence of reduced coronary perfusion
characteristic of CPR, may cause myocardial ischaemia. In addition,
prolonged CPR in the setting of very limited pulmonary blood flow
ultimately leads to progressively worsening oxygen delivery and end-
organ injury. Sano patients must overcome the significant resistance
of their lengthy pulmonary conduit and raised intrathoracic pressure
during chest compressions to achieve pulmonary blood flow. Though
Blalock-Taussig-Thomas shunted patients tend to have shorter con-
duits with less resistance, they may experience pulmonary blood flow
limitation both through raised intrathoracic pressure and poor dia-
stolic driving pressure during CPR. The diastolic pressure achieved
during CPR may be important to obtaining return of spontaneous
circulation for reasons of coronary perfusion, but it may also be
the case in single ventricle patients that diastolic blood pressure levels
are crucial for pulmonary blood flow and systemic oxygenation.
Given that IAC-CPR can augment venous return to the heart, raise
cardiac output, and improve diastolic blood pressure, the technique
could potentially increase pulmonary blood flow in both single ven-
tricle constructs. In turn, this could enhance oxygen delivery and end-
organ preservation. Such a mechanism is suggested by the findings of
this mathematical model.
This study is limited by its virtual nature, and by the assumed
inputs used which were not modelled for uncertainty and may only
approximate the in vivo condition. Because our goal was to assess
differences in physiologic parameters between IAC-CPR and stan-
dard CPR given reasonable inputs to the mathematical model, and
not to validate the model itself, we did not perform sensitivity
analyses of each physiologic component. The influence of different
parameter values could be assessed in future studies, or an alternate
single ventricle simulation model could be employed.34 As
Figure 7. Coronary perfusion pressure during IAC-CPR in Sano shunt haemodynamics.
Cardiology in the Young 5
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previously published by Babbs,20 only a half-sinusoidal function
was used for external pressures which does not account for the pos-
sibility of compression release negative pressures. However, our
model could be additionally refined to include compression data
measured by a force sensor during CPR. In the lumped parameter
construct used, the compliance of capillaries was not incorporated
as a separate circuit element. Thus, we did not account for the pos-
sible effects of capillary closing pressure on venous capacitance
(which in theory is overcome by IAC-CPR as another potential
explanation for augmented cardiac output). In reality, CPR perfor-
mance is very complicated and variable, influenced by periodic
stoppages, with physiologic parameters changing over time.
Nonetheless, IAC-CPR has been shown to be beneficial in several
adult randomised trials. This fact, in conjunction with the prepon-
derance of favourable animal data, and now our modelling infor-
mation, should justify rigorous investigation of the technique in
children. Furthermore, this study lends credence to the notion that
CPR adjunctive techniques should be considered in paediatric car-
diac patients to tailor resuscitative efforts to their unique physiol-
ogy. However, the theoretical benefits of IAC-CPR for cardiac
output in general, and coronary perfusion in specific, imply that
the methodology need not be limited to cardiac patients alone.
Non-cardiac patients may benefit from IAC-CPR once optimized
methods for children are determined, instructions are dissemi-
nated, and caregivers are adequately trained. Such work is ongoing
and may best be accomplished through multicenter resuscitation
consortia.
Conclusions
We have employed an lumped parameter model of standard CPR
and IAC-CPR in both Blalock-Taussig-Thomas and Sano single
ventricle conditions. Results indicate that IAC-CPR augments
Blalock-Taussig-Thomas shunt flow, and thus pulmonary blood
flow, by 30% compared to standard CPR; pulmonary blood flow
is also greatly increased by IAC-CPR in the Sano construct. In both
models, cardiac output was increased by IAC-CPR, avoiding a
potentially harmful steal phenomenon from the systemic circula-
tion. Similarly, coronary perfusion pressure and coronary blood
flow were increased during IAC-CPR.
This investigation is the first to advance IAC-CPR as a tech-
nique with mechanistically explicable utility in single ventricle
patients with shunt-dependent pulmonary blood flow.
Theoretical increases in pulmonary blood flow, cardiac output,
and coronary perfusion pressure/coronary blood flow during
IAC-CPR provide justification for rigorous clinical testing of the
technique in children with and without congenital heart disease.
Acknowledgements. I would like to thank my collaborators at Stanford
Engineering, Dr Alison Marsden and Dr Weiguang Yang, for their tremendous
contributions to this project and the resultant manuscript.
Financial support. This research received no specific grant funding from any
agency, either commercial or not-for-profit.
Conflicts of interest. None.
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