(Circulation. 1999;100:2146.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
CPR Techniques That Combine Chest and Abdominal Compression and Decompression
Hemodynamic Insights From a Spreadsheet Model
From Indiana University School of Medicine and the Department of Basic Medical Sciences, Purdue University, West Lafayette, Ind.
Correspondence to Charles F. Babbs, MD, PhD, Basic Medical Sciences, 1246 Lynn Hall, Purdue University, West Lafayette, IN 47907-1246. E-mail babbs{at}vet.purdue.edu
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Abstract |
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Background—This study was done to elucidate mechanisms by which newer cardiopulmonary resuscitation (CPR) techniques, including interposed abdominal compression (IAC), active compression-decompression (ACD), and Lifestick CPR, augment systemic perfusion pressure and forward flow and to compare the 3 techniques in the same test system.
Methods and Results—Mathematical models describing hemodynamics of the adult human circulation during cardiac arrest and CPR were created and exercised by use of spreadsheet software. Assumptions of the models are limited to normal human anatomy and physiology, the definition of compliance (volume change/pressure change), and Ohm’s law (flow=pressure/resistance). Standard CPR generates 1.3 L/min forward and 25 mm Hg systemic perfusion pressure. In otherwise identical models, IAC-CPR generates 2.4 L/min and 45 mm Hg; ACD-CPR, 1.6 L/min and 30 mm Hg; and Lifestick CPR, which combines IAC and ACD, 3.1 L/min and 58 mm Hg. Augmented CPR techniques work by enhanced priming of either chest or abdominal pump mechanisms.
Conclusions—Adjunctive maneuvers, combined with conventional chest compression, can produce substantial hemodynamic benefit in CPR by credible physiological mechanisms.
Key Words: blood flow • cardiopulmonary resuscitation • computers • heart arrest • Lifestick • mechanics
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Introduction |
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Two mechanical techniques have emerged from animal and clinical studies as potentially effective means of augmenting perfusion during external cardiopulmonary resuscitation (CPR). The first is the addition of interposed abdominal compression (IAC) to otherwise standard CPR.1 2 3 The second is CPR with active compression and decompression (ACD) of the chest.4 5 6 Reviews of these techniques are found in References 7 and 87 8 . During IAC-CPR, positive pressure is applied to the abdomen in counterpoint to the rhythm of chest compression, so that the abdomen is being compressed when chest pressure is relaxed. During ACD-CPR, positive and negative pressures are applied alternately to the chest by means of a "plunger" that forms a seal with the anterior chest wall. Both methods improve hemodynamics in animal studies of electrically induced ventricular fibrillation.9 10 Both improve CO2 excretion as a measure of effective systemic perfusion in human resuscitation.4 11 12 Three randomized clinical trials of IAC-CPR compared with standard CPR2 11 13 have found statistically significant benefit, and 1 early trial found no difference.14 Four randomized clinical trials of ACD-CPR have found improved outcome,5 6 15 16 and 4 other trials have found no difference.17 18 19 20 Most recently, Lifestick CPR21 has become the subject of active research. The Lifestick is a 2-handled device that is able to apply IAC and ACD-CPR simultaneously by alternately compressing and decompressing the chest and the abdomen through adhesive pads. These 3 CPR adjuncts are illustrated in Figure 1
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Using a mathematical model of CPR hemodynamics, the
nomenclature for which is given in Table 1, the author has explored the
possibility that IAC, ACD-CPR, and Lifestick CPR work by similar
mechanisms. The hypothesis is that improved filling of the thoracic
aorta and right heart can be accomplished either by positive pressure
in the abdomen or by negative pressure in the chest and conversely,
that improved filling of the abdominal aorta can be achieved either by
positive pressure in the chest or by negative pressure in the abdomen.
Improved pump filling, in turn, leads to higher stroke output, systemic
perfusion pressure, and systemic blood flow.
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The approach to the present research was to create and test a mathematical model of CPR hemodynamics based on fundamental principles of cardiovascular physiology. Such a model is independent of the many confounding factors present in laboratory studies and in clinical trials. These include varying patient populations, downtime, drug therapy, central venous pressure, peripheral vascular resistance, underlying disease, chest configuration, and body size, as well as varying rescuer size, skill, strength, consistency, prior training, and bias. Mathematical models also allow exact control of the dominant hemodynamic mechanism of CPR (thoracic pump in large subjects versus cardiac pump in small subjects).22 This approach facilitates quantitative comparison of various resuscitation techniques in exactly the same test system.
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Methods |
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Anatomic Parameters
To capture the essence of CPR hemodynamics, one may solve the family of differential equations describing pressures and flows in the simplified fluidic system shown in Figure 2
. The human circulation is
represented by 7 compliant chambers connected by
resistances through which blood may flow. The compliances correspond to
the thoracic aorta, abdominal aorta, lumped superior vena cava and
right heart, lumped abdominal and lower extremity veins, carotid
arteries, and jugular veins. In addition, the chest compartment
contains a pump representing the pulmonary vascular
and left heart compliances between the pulmonic valve and the aortic
valve. This pump may be configured to function either as a heartlike
cardiac pump, in which applied pressure squeezes blood from the heart
itself through the aortic valve, or as a global thoracic pressure pump,
in which applied pressure squeezes blood from the pulmonary
vascular bed through the left heart and into the
periphery.23 24 25
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Conductance pathways with nonzero resistances, R, connect the elastic compartments. Rh, Rht, and Rs are large and represent resistances of the systemic vascular beds of the head, heart, and trunk and legs. Rc, Ra, Rj, and Rv are small and represent in-line resistances of the great vessels. Ri and Ro are the small input and output resistances of the chest pump in series with the aortic and pulmonic valves. Niemann’s valves between the chest and jugular veins at the level of the thoracic inlet are actual but little-known anatomic structures that function to block headward transmission of large positive pressure pulses in the chest during cough and also during CPR.26
Physiological Parameters
Parameters describing a textbook normal "70-kg
man"27 (Table 2) are used
to specify values of the compliances and resistances shown in Figure 2
.
The normal 30-fold ratio of venous to arterial compliance
characterizes a circulation in the absence of fluid loading or
congestive heart failure. The distribution of vascular conductances
(1/resistance) into cranial, thoracic, and caudal components reflects
textbook distributions of cardiac output to various body regions.
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Solving for Pressures in the System
The relationships among the pressures in the various vascular
compartments are determined by the definition of compliance and by
Ohm’s law. The definition of compliance is C=
V/P, where C is
compliance and P is the incremental change in pressure within a
compartment as volume V is introduced. Ohm’s law, which relates
flow to pressure and resistance, is
i=(1/R)(P1-P2), where
P1-P2 is the instantaneous change in pressure
across resistance R as flow i occurs. In Figure 2, currents
ic (carotid), ia (aortic), is
(systemic), iv (venous), ij (jugular),
ii (pump input), and io (pump output) are shown
for clarity, with positive directions specified by arrows.
Extrathoracic Components
Applying these basic concepts with reference to Figure 2
provides a set of governing finite-difference equations that can be
used to describe hemodynamics. These equations can be
integrated numerically to describe instantaneous pressure versus time
waveforms in each of the 7 compartments. Beginning, for example, with
the abdominal aorta,
 | (1) |
Pabd represents the change in
external pressure applied to vessels in the abdominal compartment
during IAC and Lifestick CPR. For standard CPR, Pabd is
assumed to be zero. The next term represents the increase in
abdominal aortic pressure caused by net inflow of blood during the
small time interval t. Substitution for currents ia and
is by use of Ohm’s law completes the expression.
Similarly, the pressure changes in other extrathoracic vascular
compartments are given by Equations 2 through 4, as follows.
 | (2) |
 | (3) |
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 | (4) |
Thoracic Components
Corresponding expressions for the 3 thoracic components of the
model are as follows.
 | (5) |
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where E=1 during ejection (aortic valve open) and E=0 otherwise.
 | (6) |
where F=1 during the filling phase (pulmonic valve open) and F=0
otherwise, and N=0 during CPR-induced intrathoracic pressure pulses
(Niemann’s valve closed) and N=1 otherwise. Finally,
 | (7) |
Numerical Methods
Integration
Standard spreadsheet programs, such as Microsoft Excel, are
ideal for implementing numerical integration of Equations 1 through 7
to obtain pressures in all 7 compartments as a function of time. To
simulate a resuscitation, one can create a spreadsheet in which
pressures in each compartment at any point in time are computed from
the pressures at the preceding time point and the corresponding
P’s—that is,
 | (8) |
Applied Pressures for Chest and Abdominal Compression
Pchest and Pabd represent
driving intrathoracic and intraabdominal pressures applied to outer
surfaces of blood vessels in the chest and abdomen of the model.
Although any arbitrary function or waveform can be used to
represent the imposed chest and abdominal pressures in external
CPR, the present studies used half-sinusoidal functions, defined as
follows and sketched in Figure 3. To
represent chest compression,
 | (9) |
 | (10) |
 | (11) |
 | (12) |
Tpfactor1 is introduced, and a pressure
equal to the product of Pchest and Tpfactor is applied
to the thoracic aorta and superior vena cava to create a continuum of
hybrid pump mechanisms ranging from pure cardiac pump (Tpfactor=0) to
pure thoracic pump (Tpfactor=1). When Tpfactor=1, all intrathoracic
structures, including the great veins and thoracic aorta, experience a
uniform "global" intrathoracic pressure rise, as originally
conceived by Rudikoff and coworkers.28 When Tpfactor=0,
only the pump compliance, CP, is pressurized, as if the
heart alone, and not the great vessels, were compressed between the
sternum and the spine, as originally conceived by Kouwenhoven et
al.29 Intermediate values of the thoracic pump factor
allow models approximating the present
understanding,25 30 31 in which for small animals and
children, blood is impelled in external CPR predominantly by the
cardiac pump mechanism (for example, Tpfactor
0.25), whereas in
larger animals and adult humans, blood is impelled predominantly by the
thoracic pump mechanism (for example, Tpfactor0.75).
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Test Cases and Validation
The spreadsheet code was validated by solution of 12 simple test
cases for very small or very large values of the resistances and
compliances and by establishment of a model of the normal adult
circulation using Tpfactor=0. This model had an aortic blood pressure
of 120/82 mm Hg and a cardiac output of 4.9 L/min for a heart
rate of 80 bpm, closely approximating the textbook normal values of
120/80 mm Hg and 5.0 L/min.
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Results |
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Alternative CPR Methods in Adult Human Models
Figure 4a
, 4b, and 4c illustrates
5-channel pressure records after 20 cycles of CPR for the normal
human circulatory model as shown in Table 2 during a simulation of
continuous standard CPR, IAC-CPR, or ACD-CPR, respectively. In Figure 4, the peak positive abdominal pressure for IAC-CPR is 110 mm Hg,
and the maximal negative intrathoracic pressure for ACD-CPR is
-20 mm Hg, approximating published values for the 2
techniques.1 2 32 33 34 35 In this model, the thoracic pump
factor is 0.75 to simulate an adult patient in whom the thoracic pump
mechanism is dominant but there is some degree of selective cardiac
compression.25 The parameters in Table 2 were
used for this and all subsequent simulations, unless explicitly stated
otherwise. Figure 4a illustrates steady-state pressures generated by
standard CPR.
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IAC-CPR
Comparison of the pressure waveforms in Figure 4a and 4b shows the
mechanism of +110 mm Hg interposed abdominal compression CPR. The
abdominal venous pressure pulse induces increased right heart filling
pressure during IAC and consequent faster pump emptying during chest
compression compared with standard CPR. Faster pump filling is caused
by larger pressure gradients across the input valve from times 0.54 to
0.67 second of the cycle. Faster pump emptying is caused by the
Starling characteristic of the pump associated with greater filling
and, in turn, larger pressure gradients across the aortic valve during
ejection. With the addition of IAC, cardiac output increases from 1.3
to 2.4 L/min, and mean systemic perfusion pressure
(SPP=RAo-RRH) increases from 25 to 45
mm Hg compared with standard CPR. The abdominal aortic pressure
waveform (crosses in figure) leads the thoracic aortic pressure
waveform (squares) during the onset and peak of IAC, indicating
retrograde flow in the aorta. This action is similar to that of an
intra-aortic balloon pump.
ACD-CPR
Figure 4c shows steady-state pressure waveforms for
-20 mm Hg ACD-CPR. Reduced pump pressure (pulmonary
vascular pressure) during diastole promotes faster pump
filling from 0.45 to 0.60 second into the cycle. Cardiac output is
increased from 1.3 to 1.6 L/min, and mean systemic perfusion pressure
is increased from 25 to 30 mm Hg compared with standard CPR. The
ACD-induced decrease in central venous pressure offsets the ACD-induced
decrease in thoracic aortic pressure, so that augmented perfusion
pressure is maintained.
The effects on systemic perfusion pressure of IAC and ACD are similar to those reported for studies in experimental animals and in human patients.1 32 36 37 38 39 Compared with standard CPR, 110 mm Hg IAC produced an 85% increase in total flow. In the same model, -20 mm Hg ACD produced a 23% increase in total flow. The present results in an independent mathematical model confirm that the positive findings in animal studies and most clinical studies are valid and are based on the fundamental anatomy and physiology of the circulatory system.
Four-Phase Lifestick CPR
Although less well studied, Lifestick CPR is a recently developed
technique to combine the effects of IAC and ACD. The sticky,
self-adhesive compression pads of the Lifestick permit active
compression and decompression of both the chest and the abdomen.
Accurate simulation of Lifestick CPR is difficult, because actual
values of negative intra-abdominal pressure have not yet been reported.
If one estimates maximal decompression-phase pressure in the abdomen to
be -30 mm Hg, the results in Figure 4d are obtained. With this
possible 4-phase technique, mean systemic perfusion pressure is 58
mm Hg. Total forward flow is 3.1 L/min—2.5 times that of standard
CPR. Study of the pressure waveforms in Figure 4d reveals that in
4-phase CPR, negative inferior vena cava pressure draws
blood out of the chest from 0 to 0.3 second into the cycle, widening
the systemic perfusion pressure. Positive inferior vena
cava pressure from 0.33 to 0.67 second promotes excellent pump
filling.
Influence of Chest Pump Mechanisms
Systemic perfusion pressures obtained by chest and abdominal
compression are dependent on the degree to which blood is impelled by
cardiac compression versus global intrathoracic pressure fluctuation.
In Figure 5, mean systemic perfusion
pressure is plotted as a function of the thoracic pump factor for 4
possible CPR techniques: standard, IAC, ACD, and 4-phase Lifestick CPR.
Maximal compression or decompression pressures are those listed in
Table 2. Although perfusion pressures for the augmented CPR techniques
are always better than those for standard CPR, the ratios of
experimental to standard perfusion pressures vary with the thoracic
pump factor. The relative benefit of IAC-CPR compared with standard
CPR, evident in Figure 5, appears to be greater in a pure thoracic pump
model than in a pure cardiac pump model. Conversely, the relative
benefit of ACD-CPR appears to be greater in a pure cardiac pump model.
The apparent benefit of ACD-CPR is especially model-dependent and may
be greater in small-animal models, such as beagles, which permit more
cardiac compression, than in larger-animal models, including humans.
This effect might well explain the generally more dramatic and
favorable results with ACD in animal models compared with the overall
mixed results observed in humans.8
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Discussion |
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Mathematical models provide a good way to synthesize knowledge about complex systems in new and interesting ways and to explore assumptions about how the systems operate. The present mathematical model provides an independent test confirming the efficacy of adjunctive diastolic-phase maneuvers to augment perfusion during CPR. It offers a convenient and low-cost way to compare various CPR adjuncts in exactly the same test system, eliminating the need to extrapolate published results from one animal or clinical model to another. The results confirm that compression and decompression of either the chest or the abdomen can move blood in cardiac arrest. Importantly, the positive effects of IAC-CPR, ACD-CPR, and 4-phase Lifestick CPR can be predicted from fundamental principles of cardiovascular physiology—the definition of compliance and Ohm’s law.
Analysis of pressure waveforms suggests that these techniques function primarily by pump priming. In IAC-CPR, the chest pump is primed by positive pressure in the abdomen during thoracic recoil. In ACD-CPR, the chest pump is primed by negative diastolic pressure in the chest that draws blood centrally from extra-thoracic veins. In 4-phase Lifestick CPR, these effects are combined so that negative thoracic and positive abdominal pressures prime the chest pump. In turn, positive thoracic and negative abdominal pressures prime the abdominal pump.
Conclusions
The present mathematical model, based on fundamental aspects
of cardiovascular physiology, provides a recapitulation
and synthesis of abundant experimental and clinical evidence suggesting
that adjunctive compression and decompression of the chest and abdomen
can improve current standard CPR. Systemic perfusion pressure
achievable with IAC alone is approximately double that of standard CPR.
Systemic perfusion pressure achievable with full 4-phase CPR might
possibly exceed 3-fold that of current standard CPR. Improved perfusion
during IAC-CPR may not necessarily lead to better long-term survival,
especially when the underlying rhythm is asystole or electromechanical
dissociation.13 For the fraction of cardiac arrest victims
who can be saved, however, these techniques, performed by trained
healthcare providers, are valid and practical alternatives to standard
CPR and have a rational place in resuscitation protocols of the 21st
century.
Received April 20, 1999; revision received June 29, 1999; accepted July 9, 1999.
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