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Chest Compression Technique

A Neglected Key to Success
in Cardiopulmonary Resuscitation

Charles F. Babbs, MD, PhD

CONTENTS
INTRODUCTION
PHYSIOLOGY OF CHEST COMPRESSION IN CPR
TECHNIQUE OF CHEST COMPRESSION IN CPR
INTERRUPTION OF CHEST COMPRESSIONS FOR VENTILATION
CONCLUSIONS
REFERENCES

INTRODUCTION
The concept of external cardiac massage, first introduced in the early 1960s by
Kouwenhoven, Jude, and Knickerbocker (1), includes chest compressions at a rate of 60
to 100 per minute in conjunction with mouth-to-mouth rescue breathing (2). Refinements
of standard cardiopulmonary resuscitation (CPR) since its introduction in the 1960s have
included increasing the rate of chest compression from 60 per minute to 100 per minute,
which research makes little difference in blood flow (3), and recently decreasing the tidal
volume of the positive pressure ventilations under certain circumstances (2,4). Elimination of the carotid artery pulse check in the year 2000 guidelines has abolished an unnecessary delay in starting chest compressions by lay rescuers. Yet for many of us, chest
compression remains the centerpiece of resuscitation from full cardiopulmonary arrest,
and there has been precious little investigation of how to do it properly.
Today, the optimization of chest compressions in CPR remains a grossly neglected
area of research and practical training. The definition of proper chest compression technique is open to question, regarding such basic aspects as depth, rate, and the ventilation
to compression ratio. Only one systematic study of compression depth has been published (5). The importance of a particular compression rate is generally over emphasized,
and overrated, despite research evidence showing that rates in the range of 60 per minute
to 100 per minute are about equally effective. Several thoughtful investigators have
suggested and demonstrated in practice that chest compression only CPRwithout
any ventilationscan be equally effective or more effective than standard CPR (612).
From: Contemporary Cardiology: Cardiopulmonary Resuscitation
Edited by: J. P. Ornato and M. A. Peberdy Humana Press Inc., Totowa, NJ

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Even if one accepts that current guidelines describe correct chest compression technique, several studies have shown that chest compressions are improperly performed by
most lay rescuers and many health care workers as well (1315).
The time has come for serious efforts to optimize guidelines for chest compression and
to implement those guidelines effectively in the field. This chapter reviews the mechanisms by which chest compressions generate blood flow in CPR, the scientific basis for
effective techniques of chest compression, the issue of unnecessary interruptions of chest
compressions, and the optimal ventilation to compression ratio in CPR.

PHYSIOLOGY OF CHEST COMPRESSION IN CPR

Chest compressions can move blood during cardiac arrest (CA) and CPR by two
different mechanisms. These are known as the cardiac pump and the thoracic pump. The
cardiac pump mechanism was the first to be recognized by the original discoverers of
closed-chest CPR (1). This pump mechanism is operative to the extent that external chest
compression squeezes the cardiac ventricles between the sternum and the spine. As a
result, forward blood flow occurs through the aortic and pulmonic valves without mitral
or tricuspid incompetence. In particular, when the cardiac pump mechanism is operative
in CPR, the aortic valve is open and the mitral valve is closed during chest compression
(16). The cardiac pump mechanism is also operative during open-chest cardiac massage.
The thoracic pump mechanism was discovered in the 1980s as a result of Crileys
clinical observation of cough CPR (17,18) and extensive laboratory studies at Johns
Hopkins University, led by Myron Weisfeldt and coworkers (19,20). This pump is
operative to the extent that chest compression causes a global rise in intrathoracic pressure sufficient to force blood from the pulmonary vasculature, through the heart, and into
the periphery. When the thoracic pump mechanism is operative both the mitral valve and
the aortic valve are open simultaneously during chest compression (2123). In this situation, the left heart acts as a conduit, and the collective pulmonary vasculature constitutes
the main pumping chamber that fills and empties.
A hybrid pump mechanism can also occur in which the global intrathoracic pressure
within the pulmonary capillaries, venae cavae, and aorta is intermediate between the
values that would appear during thoracic pump CPR and those that would appear during
cardiac pump or open chest CPR. Indeed current dogma suggests that such a combined
pump mechanism is operative in most persons. In adults, the hybrid pump is predominantly thoracic and in children the hybrid pump is predominantly cardiac (24).
The reasons why these pumps work are not rocket science. They can be demonstrated
in relatively simple mathematical models that represent the essential features of the
human cardiovascular system (2530). Understanding of the relevant physiology has
led to inventiveness. Over the past 20 years a variety of ways of enhancing pump
function have been explored and are discussed elsewhere in this volume. High impulse
CPR, for example (3133), aims to enhance the action of the cardiac pump mechanism.
Vest CPR (34,35) aims to enhance the action of the thoracic pump mechanism through
the action of a pneumatic vest that is rapidly inflated and deflated at a rate of 60 to 150
times per minute. Active compressiondecompression CPR (36,37) aims to improve
filling of the either the cardiac pump or the thoracic pump by creating negative pressure
in the thorax during decompression. Interposed abdominal compression CPR (3842)
aims to improve priming of either chest pump through active abdominal counterpulsation. These methods have been called CPR adjuncts, because they usually require the

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Fig. 1. Pressures in a mathematical model of the normal adult human circulation with the cardiac
ventricles beating. The heart rate is 80 per minute. Pressures are plotted as a function of cycle time
in the thoracic aorta, Pao; the right atrium, Prh; the intrathoracic pump, Ppump, here the left ventricle.
Mean coronary perfusion pressure (CPP) is calculated as Pao minus Prh. CPP is 95 mmHg. Forward
flow is 5.0 L per minute.

deployment of an extra rescuer or device, with the hope of improving perfusion during
CPR. The focus of the present chapter, however, is on ordinary, conventional chest
compression, which is often done poorly at best.
One easy way to demonstrate and study the physiology of blood flow during chest
compression is through a mathematical model of the circulation that includes both cardiac and thoracic pumps (30). In such a model, only a small number of assumptions is
required to obtain realistic results (30). These are limited to (a) the existence of compliant
vessels and resistive vascular beds; (b) the definition of compliance (6V/6P); (c) normal
anatomy, that is the arrangement of connected vessels and cardiac chambers; and (d) a
linear relation between flow and pressure (i.e., Ohms Law flow = pressure/resistance).
Although much more complex models of the circulation can be created, only these basic
assumptions are needed to demonstrate the mechanisms of blood flow during CPR.
Circulatory systems that have these properties will behave similarly, including those of
large and small people and experimental animals. The exact values of vascular compliances and resistances, as well as other technical details of a working model, which can
be implemented in a Microsoft Excel spreadsheet, are fully described elsewhere (30).
As a point of reference and calibration, Fig. 1 illustrates pressures in a simplified
cardiovascular system for a nonarrested circulation of a hypothetical 70 kg man. Here a
cardiac pump generates left ventricular pressures (Ppump) of 122/2 mmHg at a heart rate
of 80 per minute. Systemic arterial blood pressure is 119/82, mean arterial pressure is 95
mmHg, and cardiac output is 5.0 L per minute. These are classical textbook values for the
normal human circulatory system (30). Note the essentially normal arterial pulse waveforms and low systemic venous pressures. The data point representing the exact minimum, diastolic pressure at 82 mmHg is not plotted on the chart.

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Fig. 2. Pressures in a mathematical model of the normal adult human circulation during CA and
CPR with a pure cardiac pump mechanism. The compression rate is 80 per minute. Intrathoracic
pressure acting on the cardiac ventricles ranges from 0 to +60 mmHg with a half sinusoidal
waveform. Other pressures are defined as in Fig. 1. Forward flow is 2.5 L per minute, and CPP is
47 mmHg.

Cardiac Pump CPR

Figure 2 illustrates the action of a pure cardiac pump CPR in the same circulatory
model during CA. Steady-state conditions are shown after stable pressures have been
achieved by 20 prior compressions. In this simulation only the right and left ventricles
of the heart are compressed at a rate of 80 per minute with a half sinusoidal waveform
having a peak pressure of 60 mmHg, a typical value reported in the literature of standard
CPR (28). There is no intrinsic myocardial contractility in this system, and there is no
pump priming effect of atrial contractions (which in some circumstances could exist for
a few minutes in witnessed arrests). The cardiac pump produces reasonable aortic pressures and very small venous pulsations. These are pressures that the CPR pioneers of the
1960s had in mind when they conceived of external cardiac massage. Note especially
the low right-sided central venous pressures. There is substantial coronary perfusion
pressure (aortic to right atrial gradient) throughout the compression cycle. Forward flow
is 2.5 L per min, and systemic perfusion pressure is 47 mmHg. This state of affairs
represents idealized classical external CPR in which the heart is squeezed between the
sternum and the spine as reported in 1965 by DelGuercio (43). It is also a reasonable
representation of open chest CPR with manual cardiac compression (4447), which
obviously works by a pure cardiac pump mechanism. A similar state of affairs can
occur in children (and young pigs [48,49]), who have small compliant chest walls.
Figures 1 and 2 were generated using positive applied extravascular pressures during
the compression phase and extravascular pressure during the relaxation phase. A relatively recent concept in the physiology of CPR is the use of active decompression, rather
than simple relaxation, between chest compressions. Decompression can be accomplished by the use of plunger-like devices (discovered accidentally using a real toilet
plunger! [36,50]) or by sticky adhesive pads that make contact with the skin of the
anterior chest or abdomen such as those incorporated into the Lifestick device (51). This

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Fig. 3. Sketch of active compressiondecompression cardiopulmonary resuscitation using a

plunger-like device. Active decompression at a minimum ensures full chest wall recoil and promotes blood return to the chest.

Fig. 4. Pressures in a mathematical model of an adult human during cardiac arrest and active
compressiondecompression cardiopulmonary resuscitation with a pure cardiac pump mechanism. The compression rate is 80 per minute. Intrathoracic pressure acting on the cardiac ventricles
ranges from 0 to +60 mmHg with a half sinusoidal waveform. Maximal decompression pressure
is 20 mmHg. Other pressures are defined as in Fig. 1. Forward flow is 3.2 L per minute and
coronary perfusion pressure is 61 mmHg.

approach is known as active compressiondecompression CPR (ACD-CPR; Fig. 3).

Today, active decompression of the chest during CPR can be accomplished using a
specially designed plunger applied to the human sternum (47,5254), which is sold
commercially in Europe as the Ambu Cardiopump.
Figure 4 illustrates the steady-state effect of active decompression of the chest to negative 20 mmHg, the maximum reported in the literature (52,55,56). This particular simulation is for cardiac pump CPR. Combining both positive and negative chest pressures has a
salubrious effect on hemodynamics. Cardiac filling is enhanced during the negative pressure phase, so that greater stroke output can be achieved on the next positive pressure phase.

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Fig. 5. Pressures in a mathematical model of the normal adult human circulation during cardiac
arrest and cardiopulmonary resuscitation with a pure thoracic pump mechanism. The compression
rate is 80 per minute. Global intrathoracic pressure acting on the cardiac ventricles, right heart,
venae cavae, and thoracic aorta ranges from 0 to +60 mmHg with a half sinusoidal waveform.
Other pressures are defined as in Fig. 1. Forward flow is 0.93 L per minute; CPP is 18 mmHg.

Note in Fig. 4 the particular times near 0.55 seconds in the cycle when pump pressure is
substantially less than right heart pressure. At this stage enhanced pump filling occurs. The
result of enhanced pump filling is greater forward flow and greater perfusion pressures
3.2 vs 2.5 L per minute and 61 vs 47 mmHg.
An effect similar to active decompression may be obtained with conventional CPR,
properly performed with no leaning on the chest. Especially in a younger individual there
is natural recoil of the ribs after compression (in the absence of chest wall breakdown or
broken ribs). This recoil helps to create transient negative pressure in the chest that promotes pump filling. Poorly performed external CPR with leaning on the chest inhibits this
normal passive decompression. One can also regard Fig. 4 as a model of ordinary chest
compression in a young adult, performed by a rescuer who allows full chest recoil between
down strokes. Only when filling is unimpeded can chest compression be effective. Otherwise, compression of pumping chambers that are already empty produces little flow.

Thoracic Pump CPR

When it works, the cardiac pump mechanism is the most effective and natural of the
three pumps in CPR (cardiac, thoracic, and abdominal [27]). Its operation in external
CPR, however, depends on good mechanical coupling between the sternum and the heart.
In most adults the coupling of chest compression to the heart is indirect, and a thoracic
pump mechanism tends to predominate (23,24,34).
Thoracic pump CPR has a quite different set of pressure profiles. Figure 5 illustrates
the action of a pure thoracic pump. In this simulation all intrathoracic blood containing

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Fig. 6. Active decompression with thoracic pump cardiopulmonary resuscitation. The compression
rate is 80/min. Intrathoracic pressure acting on the cardiac ventricles ranges from 0 to +60 mmHg
with a half sinusoidal waveform. Other pressures are defined as in Fig. 1. Maximal chest compression pressure is +60 mmHg. Maximal decompression pressure is 20 mmHg. Here forward flow
is 1.1 L per minute and CPP is 22 mmHg.

chambers are pressurized equally at a rate of 80 per minute with a peak pressure of 60
mmHg, as before. This state of affairs happens in broad chested older individuals. It also
happens during vest CPR, in which a pneumatic vest encircles the chest to produce pulses
of compression from all sides simultaneously.
In thoracic pump CPR forward flow occurs even though the heart is not being squeezed
between the sternum and the spine. Coronary blood flow and systemic blood flow occur
when aortic pressure is greater than systemic venous or right heart pressure. As shown
in Fig. 5, positive coronary and systemic perfusion pressures occur mostly during diastole, between compressions, rather than during systole (i.e., during compressions).
Phase differences in central arterial and venous pressure waveforms may allow limited
systolic perfusion as well. Because of the tendency toward equalization of aortic and
venous pressures during systole, forward flow with the thoracic pump mechanism tends
to be less than with the cardiac pump mechanism, other factors being equal. In the
thoracic pump model of Fig. 5 forward flow is only 0.94 L per minute and systemic
perfusion pressure is 18 mmHg.
If an active decompression phase is added (Fig. 6), perfusion pressures are somewhat
increased, but to a lesser extent than with cardiac pump CPR. Now forward flow is 1.14 L
per minute and systemic perfusion pressure is 22 mmHg. Herein lies the challenge of
performing external chest compressions in adults. One must generate not only pressure
pulses, but also forward flow of blood. The chances of doing this are improved by using
a thoughtful technique based on research findings from the animal laboratory and the
clinic.

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Fig. 7. Relative forward flow in cardiopulmonary resuscitation (CPR) as a function of compression depth, as reported in the animal studies of Fitzgerald et al. (3). As compression depth during
Thumper CPR increased, flow increased in each animal. However, no flow was obtained at
compression depths less than 2 cm. The solid line is a least squares linear regression to data from
eight anesthetized dogs.

TECHNIQUE OF CHEST COMPRESSION IN CPR

Amplitude or Depth of Compression
Current guidelines for CPR state that chest compressions be performed to a depth of
1.5 to 2 inchesapprox 4 to 5 cm. This recommendation is based on the experience of
early pioneers of CPR. There are no clinical data in humans that describe what happens
to blood flow when chest compressions are between 0 and 1.5 inches (how bad is too
little), when chest compressions are between 1.5 and 2 inches (how stable is the target
region), or when chest compressions are greater than 2 inches (how much more can be
squeezed out of the system and at what cost in complications). The vigor of manual chest
compression may vary widely among rescuers and may progressively diminish as a given
rescuer tires. The effects of these variations are unknown, but would be inconsequential
only if the function relating blood flow to chest compression depth showed a broad
plateau in the neighborhood of 1 to 2 inches.
In the only existing study of the relationship of blood pressure and flow during CPR
to chest compression amplitude, small (612 kg) anesthetized dogs were resuscitated
during 2-minute periods of electrically induced ventricular fibrillation (VF) and
Thumper CPR (3). Cardiac output was measured using a special indicator dilution method
designed for accuracy during the low-flow conditions of CPR. The results (Fig. 7) showed
anything but a plateau. Chest compressions exceeding a threshold value (x0) between 1.5
and 3.0 cm were required in each animal to produce measurable cardiac output. Cardiac
output increased as a linear function of compression depth beyond the compression
threshold. That is CO = a(x x0) if x > x0 for chest displacement, x, and constant, a.
However, if x < x0 CO = 0.
The mean value of x0 was 2.3 cm, a value very close to 1 inch (2.54 cm). A similar
threshold of 1.8 cm was found for measurable blood pressure in response to chest compression. For chest compression depths greater than 2.5 cm relatively modest increases

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Fig. 8. Conceptual models of forward flow in cardiopulmonary resuscitation as a function of

compression depth. A = plateau function implied in the guidelines. B = actual function from
laboratory studies, including the effective compression threshold at 2 cm.

in chest compression caused relatively large increases in cardiac output (Fig. 7). These
observations are supported by clinical experience, as well (57). Experienced rescuers
have learned that in some persons 1 to 2 inches of sternal compression may be inadequate
and a slightly greater degree of chest compression may be needed to generate an adequate
carotid or femoral pulse. Authorities suggest in the guidelines for basic life support that
optimal sternal compression is best gauged by using the compression force that generates
a palpable carotid or femoral pulse. Yet we know from physiology and from tracings such
as Fig. 5 that pressure pulses do not guarantee blood flow if the venous and arterial pulses
are the same.
Current guidelines for compressions to a depth of 1.5 to 2 inches or 4 to 5 cm are
supported by limited research data. However, the guidelines and associated teaching
materials do not emphasize the depth of compression as a critical variable. Rather, they
seem to imply that any degree of chest compression within the prescribed range of 1.5 to
2 inches is satisfactory. Such an interpretation would be rational if the true function
relating cardiac output and compression depth were as shown in Fig. 8, curve A. This
hypothetical function rises to a plateau, such that any degree of compression in the plateau
region would be close to maximally effective.
Research data (Fig. 7) however, argue strongly that the actual functional relationship
is more like that of line B in Fig. 8. In this situation flow is quite sensitive to small changes
in sternal displacement, and for some displacements below a critical threshold value,
cardiac output is virtually nil.
Under field conditions in which the force and depth of chest compression may vary,
it is unlikely that a given victim receives optimal CPR for the duration of the resuscitation
effort. Chest compression may drift below the effective compression threshold as rescuer
fatigue sets in. The steepness of the slope of the actual flow vs compression depth line,

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cries out for a more effective monitor of chest compression during CPReither a monitor
of compression depth itself, or better still, a monitor of blood flow or organ perfusion, so
that professional rescuers could use biofeedback to maintain effective chest compression
throughout the duration of a resuscitation effort.
Of course, there is potential harm form more forceful chest compressions that must be
balanced against the hemodynamic benefit. In a previous study Redding and Cozine (44)
found that during closed chest massage in dogs, mediastinal hemorrhage, fractured ribs,
and lacerations of the liver were frequently encountered when maximal force was applied
to the chest sufficient to produce the greatest possible blood pressure. However, Redding
and Cozine quickly developed a moderately forceful technique that generally avoided
these complications.
Current CPR has been likened to flying a 747 aircraft without instruments. The
existence of an effective chest compression threshold is a powerful reason for more effective monitoring of circulation during CPR on a routine basis. One simple expedient, in lieu
of future high tech monitors is placement of a long soft rubber tube, filled with water, in
the esophagus for pressure monitoring. This system can be completely safe if a cuffed
endotracheal tube is in place. When pressure pulses generated in the esophageal tube are
50 mmHg or greater, nearly maximal cardiac output is obtained in laboratory experiments
(5). Greater forces are ineffective in generating greater flow; hence the 50-mmHg esophageal pressure rule provides a convenient yardstick for optimal chest compression. Unfortunately, this simple and low cost approach has yet to be implemented clinically.
A new and interesting twist on monitoring of chest compressions is a device incorporated into the chest compression pad of the Zoll AED-Plus automatic external defibrillator. The sternal chest compression pad, located between stick-on defibrillating
electrodes includes a miniature accelerometer. The signal from this electronic device is
doubly integrated to produce a measure of compression depth that is monitored by the
device. Auditory feedback can be provided to the rescuer if chest compression depth, so
monitored, falls outside the recommended range. Technical aids such as this one may
improve the quality of external chest compressions in the future. Although not a physiologic end point, compression depth, accurately displayed to the rescuer on a push-bypush basis would at least improve consistency and control over an important independent
variable in the physiologic equation of CPR.

Compression Rate
Kevin Fitzgerand et al. conducted an extensive laboratory study in anesthetized dogs
of compression rate using a specially designed, computer-controlled Thumper (a piston
for chest compression driven by compressed gas). Fitzgerald et al. measured cardiac
output during electrically induced VF and CPR as the major dependent variable, using
a technique adapted to low-flow conditions. Chest compression rates ranging from 60 to
120 per minute were equally effective in this model. A mathematical curve fit to the data
yielded a function beginning appropriately with 0 flow at 0 compression rate and rising
to a plateau between 60 and 120 compressions per minute. In the plateau region there was
about a plus or minus 20% variation in flow, with little evidence suggesting that one
compression rate was better than another (Fig. 9).
This empirical result has also been demonstrated in analog computer models of the
circulation (27). In the plateau region stroke volume of the chest pump diminishes with
increasing chest compression rate, much as that of the natural heart. The reason is prob-

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Fig. 9. Relative cardiac output as a function of compression rate after Fitzgerald et al. Range of
relative flows based on 20 to 30 determinations in 10 animals is plotted in terms of the 1 SD
values, where SD denotes 1 standard deviation from the mean. 1.0 on the ordinate represents
42 mL per minute per kg body weight. In the range of 60 to 120 compressions per minute there
is little effect of compression rate.

ably the samereduced pump filling with shorter cycle times. When it comes to compression rate, unlike compression amplitude, the functional curve really does have a
plateau. Hence one could say that current teaching of basic life support has it backwards
regarding which variable is critical. We should not be stressing that trainees achieve a
particular target rate in doing chest compressions, although any compression depth in the
range of 1.5 to 2 inches is acceptable. We should be stressing that compression depth is
the critical variable, and any rate between 60 and 100 per minute is acceptable.
DUTY CYCLE OR COMPRESSION DURATION
It was my mentor, Dr. Leslie Geddes, an award winning biomedical engineer, who
introduced the term duty cycle into the literature of CPR. Duty cycle is defined as the
ratio of compression duration to total cycle time. For example, the recommended duty
cycle for standard CPR is 50%half compression, half relaxation. In the animal laboratory Fitzgerald et al. also studied the effects of changes in duty cycle at a variety of
compression rates with the programmable Thumper. For anesthetized dogs in electrically induced VF Fitzgerald et al. found inverted U-shaped functions at all rates (Fig. 10).
Peak flow occurred between 30 and 50 and duty cyclethat is 30 to 50 and compression
duration. Other investigators using other models have confirmed these results. For
example, Babbs and Thelander (58), using a mathematical computer model of the
human circulation, found that total pulmonary artery flow and coronary artery flow
peaked at 30 to 40% duty cycle for standard CPR. Interestingly, cranial flow to the brain,
unlike that to other organs, peaked at near 60% duty cycle, in keeping with the observation of Taylor, Weisfeldt, and coworkers (59), who measured ultrasonic doppler flow
velocity index in carotid arteries of anesthetized dogs and in carotid arteries of humans
during CPR.

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Fig. 10. Average values of relative cardiac output as a function of duty cycle of compression at
60 per minute and 120 per minute compression rate. Data are from Fitzgerald et al. Here each
animal served as its own control. The effects of duty cycle are independent of rate in the range of
60 to 120 compressions per minute.

Taylors study proved to be historically influential in standards writing. In response

to the evidence that increased duty cycle created better brain flow, standards writers
decided to increase the recommended rate of compression, because practical rescuers
tended to compress the chest with a fixed duration of about one-third of a second. Increasing rate, assuming the compression duration is constant, automatically increases the duty
cycle without requiring learns to alter two different aspects of their technique. Unfortunately this change, together with subsequent rate increases in the year 2000 guidelines,
failed to account for the effect of faster compression rates on total cardiac output when
compression-to-ventilation ratios are kept the same. This interesting and controversial
subject is discussed fully in the final section of this chapter.
HAND POSITION ON THE CHEST
Proper hand placement for chest compression has been established through clinical
experience rather than through systematic research. The compression point has become
accepted as the middle of the lower half of the sternum. In studies of cardiac angiography
during CPR (60) this location appeared to be most effective. However, if compression is
centered too high, that is too far cranial, in the upper half of the sternum, the aortic and
pulmonary artery roots are squeezed and kinked at the base of the heart, actually obstructing outflow. In this situation forward flow is close to 0. If compression is centered too low,
the xiphoid process may be driven into the left lobe of the liver, resulting in liver laceration. If the compression point is shifted laterally the costochondral junctions may be
subluxed or ribs may be broken.*
*I have become aware of anecdotal reports of more effective CPR when the compression point
is shifted left of midline to a position over the left ventricle. The method is said to produce a
facial flush, indicative of dramatically improved blood flow, and to have achieved a handful
of dramatic rescues. However, reports of the technique, known as the Williams maneuver after
its inventor, have not yet appeared in the peer-reviewed literature.

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Typically, the long axis of the heel of the rescuers hand is placed on the long axis of the
lower half of the sternum. This alignment helps to keep the main force of compression on
the sternum and to decrease the chance of rib fracture. The fingers may be either extended
or interlaced but should be kept off the chest, again to reduce chances of rib fracture. An
acceptable alternative hand position is to grasp the wrist of the hand on the chest with the
opposite hand. This technique is helpful for rescuers with arthritic hands and wrists (57).
It is important not to lift the hands from the chest or change position frequently,
otherwise correct hand position may be lost. However, it is also important not to lean on
the chest, maintaining forceful contact during the release phase, because this action limits
venous return to the pump. Bouncing compressions, jerky movements, improper hand
position, and leaning on the chest can decrease the effectiveness of resuscitation and are
more likely to cause injuries. To ease fatigue of the triceps muscles, the elbows should
be locked into position, with arms straightened, and shoulders positioned as directly over
the hands as possible, so that the thrust for each chest compression is straight down on
the sternum. If the thrust is not vertical, the torso has a tendency to roll; part of the
downward force is displaced, and the chest compression may be less effective.
BIOMECHANICS OF RESCUER ACTION
After all this positioning, which mercifully takes much longer to read than to perform
in actual practice, it is now time to begin chest compressions. Classically (57) rescuers
have been taught to lean forward with the shoulders until they are directly over the
outstretched hands. That is to lean forward until the body reaches natural imbalance
a point at which there would be a sensation of falling forward if the hands and arms were
not providing support. With this technique the weight of the trunk creates the necessary
force to depress the sternum; arm strength is not required.
The approach just described works well for the down stroke. However, an up stroke
or recovery phase is also important and is needed to complete the full cycle. Unfortunately, a fatigue-generating problem can easily occur during the recovery phase of rescuer action. The problem is that when one leans forward from the waist, the obvious
recovery stroke is to lift up the torso from the waist using the back muscles (erector spinae
complex), which in humans are relatively weak and prone to fatigue, as well as prone to
painful spasm at the most unfortunate of times.
A LEARNING ACTIVITY, PART 1
To understand the importance of this point deeply, try standing up and bending forward enough to touch your knees with your hands and then lifting your shoulders back
to a standing position at the recommended rate of 100 times in 60 seconds. Do not be shy.
Try this right now; it is part of the book chapter. Notice that you had difficulty doing all
100 bends in the time allowed. Notice the feeling of fatigue, if not pain in your back
muscles. Notice your feeling of anger at my making you do this. Indeed people who use
this approach on a chest or manikin find it so difficult that they soon tend to allow the chest
recoil push their own torso weight upward to save energy. That is they lean on the chest
to compensate for the imbalance. Unfortunately for the patient this action results in
greater diastolic (recovery phase) force on the chest than is needed. This extra force
impedes chest pump filling and reduces the effectiveness of CPR. Some of the effectiveness of active compression-decompression-CPR may simply be a result of its allowing
natural chest recoil to occur, rather than allowing the individuals chest recoil to rescue
the rescuer from fatigue!

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A LEARNING ACTIVITY, PART 2

Now try the following experiment, which is much more pleasant than the first one.
Although standing, bend your knees slightly to lower your hips and torso as a unit through
a distance of 5 cm toward the floor and return to a standing posture. Repeat this cycle 100
times in 60 seconds. Keep your back straight, head up, and shoulders back. Look forward
and just bounce up and down 5 cm each time. You probably noticed how much easier this
exercise is than bending over. It is certainly no more tiring than jogging or running in
place or dancing. It is also much easier to do at a faster rate approaching 100 per minute.
There is even some energy return from the legs during upward motion, because of natural
recoil of tendons and muscles of the legs. Here the muscles that are doing the work are
the quadriceps femoris muscles of the anterior thighsthe largest and most powerful
muscles in the human body. This is a better way to do CPR.
Now consider the following biomechanically efficient approach to chest compression.
This technique produces reduced back fatigue for the rescuer and greater effectiveness
for the individual. The rescuer either kneels beside the thorax of the individualas close
as possibleor works astride the individual on his or her knees. If the patient is raised
on a table, a stool may be needed by the rescuer to provide the necessary elevation. The
arms should be straight and as vertical as possible, and the elbows should be locked, as
before. In this position the rescuer can work effectively by raising and lowering the hips
(not the shoulders) against gravity, using the anterior thigh muscles, NOT the back.
As the rescuers hips are lowered in the kneeling position with the back straight and
firm, the weight of the rescuers body can be used to apply compression. As the rescuers
hips are raised the quadriceps muscles of the anterior thigh can work to complete the
cycle, although the rescuers arms remain straight. As a final exercise the reader is
encouraged to try this motion in the kneeling position while palpating the quadriceps and
hamstring muscles. Note that when the hips are raised when kneeling, the leg is extended
at the knee joint by the quadriceps and the thigh is extended at the hip joint by the
hamstrings. Posterior compartment (hamstring) muscles are active as well in the kneeling position. Reliance on the strong anterior and posterior thigh muscles minimizes
fatigue and keeps the exercise aerobic for either male or female rescuers. These same
muscles should be used as much as possible in the standing position as well. Upper body
strength is not required, once rescuers learn to use leg muscles and NOT back muscles.
Even with this more biomechanically efficient technique, adequate personnel need to be
available, whenever possible, so that frequent changes can occur every 35 minutes to
avoid fatigue. As fatigue sets in, rescuers tend to revert to former habitual methods of
chest compression, which are less effective.
A FINAL NOTE REGARDING THE RELEASE PHASE
The release phase of chest compression is just as important as compression itself.
Release chest compression pressure between each compression to allow blood to flow
into the chest and heart. The pressure must be released and the chest must be permitted
to return to its normal position after each and every compression. Chest recoil is considered by thoughtful students of CPR physiology to be critical in promoting venous return
to the chest pump and proper filling for the next cycle.

CPR Performed on a Soft Surface Such as a Mattress

Because the effectiveness of chest compression during standard CPR may be seriously
degraded on soft supporting surfaces such as hospital beds; it is standard practice to place

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a backboard under the patient to provide a more unyielding surface. According to guidelines for basic life support (4): If the individual is in bed, a board, preferably the full
width of the bed, should be placed under the patients back to avoid the diminished
effectiveness of chest compression. For those patients who are large or who are connected to many monitoring and life support devices, the placement of a backboard can be
difficult and time consuming. Sometimes the patient is moved to the floor, requiring
interruption of CPR. Sometimes backboards are not immediately available, or there is a
delay in finding one. Under these circumstances rescuers must make do with a modified
technique.
One approach is to use a modified compression technique for soft surfaces developed
by Boe and Babbs, who conducted a systematic mechanical analysis of the effects of
substrate stiffness on chest compression in CPR (61). Their modified technique is
called the constant peak force technique. With this approach the rescuer concentrates
on the force applied, rather than the distance moved by the compressing hands. The
rescuer compresses the sternum using the same maximum force regardless of any
patient motion. This mode is similar to that applied by the Thumper mechanical
resuscitator, and also by smaller adult rescuers who focus on using body weight to apply
chest compressions.
The constant peak force technique helps to compensate for underlying bed softness
vs chest stiffness. In Boe and Babbs analysis if the rescuer used a conventional constant
5 cm peak displacement, sternum-to-spine compression fell from 4.3 to 1.0 cm, as
underlying bed stiffness decreased from 50,000 to 5000 N per meter. At a typical bed
stiffness of 10,000 N per meter less than 35% of intended chest compression occurred.
At the same time peak power exerted by the rescuer fell to about half that for a hard
surface, because it is easier to compress a mattress than an adult human chest. However,
if a constant peak force of 400 N was applied, regardless of the observed displacement
of the chest and bed, greater than 85% of maximal chest compression was obtained at
a typical bed stiffness of 10,000 N per meter. The cost of the increased effectiveness was
that the power exerted by the rescuer was approximately double that required on a hard
surface. That is, the rescuer had to work harder because he or she was compressing both
the mattress and the patient.
The good news is if necessary, CPR can be performed effectively on a softer surface
using a constant peak force technique. Although a firm surface is most desirable, the
constant peak force technique is capable of maintaining a significant degree of chest
compression on all but the softest surfaces, albeit at the expense of greatly increased work
by the rescuer. This approach may be quite useful in coronary care unit settings, for
example, when arrests are brief, lines and cables are numerous, and electrical defibrillation is readily available.

INTERRUPTON OF CHEST COMPRESSIONS FOR VENTILATION

Current adult CPR by one or two rescuers is based on the traditional ABCsairway,
breathing, circulationwith a 15:2 compression to ventilation ratio (2). That is, the
rescuer compresses the chest 15 times, pauses to give two mouth-to-mouth ventilations,
and then continues with chest compressions. The former convention of 5:1 compression
ventilation ratio for two-rescuer CPR has been dropped in the most recent guidelines
for the sake of simplification and coordination between North American and European
practice.

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The 15:2 ratio is essentially the same as the normal ratio of heart rate to breathing
in a quietly resting adult with a heart rate of 75 beats per minute and a respiratory rate
of 10 breaths per minute, namely 7.5:1 or 15:2. Recently, the issue of the most desirable
compression to ventilation ratio has been reopened because of the reluctance of many
rescuers, both lay and professional, to perform mouth-to-mouth rescue breathing, owing
to the fear of contracting serious communicable diseases such as AIDS (6264). Moreover, the relatively long pauses in chest compression required for ventilation lead to
disturbingly long interruptions in chest compressions and associated blood flow. In turn,
the average systemic perfusion pressure over a complete compression/ventilation cycle
may be much lower than is generally appreciated.
Consider, for example, a set of 15 compressions at a compression rate of 100 per
minute (2), which requires 9 seconds to deliver. If a rescuer takes 5 seconds to administer two slow, deep rescue breaths of 700 to 1000 mL each, as specified in current
guidelines (2), then chest compressions are only being delivered 9/14ths of the time.
The 5-second pause for ventilation following every 15 chest compressions has been
shown in experimental models to reduce coronary perfusion pressure by 50% (10). This
loss of perfusion pressure must be rebuilt during each subsequent set of compressions,
and typically requires about 5 to 10 compressions before the previous level is achieved
(10). In some cases the 5-second pause for ventilation may reduce overall mean systemic perfusion below the value of approx 25 mmHg required for effective resuscitation
(6567).
In the real world, interruptions of chest compressions get worse. Recent videotape
analysis of lay rescuers in action shows that the interruption of chest compression for
rescue breathing consistently requires about 16 seconds to perform (68,69). The act of
delivering two slow, deep rescue breaths is not just blowing into the mouth of the individual, but the physical task of stopping compressions, leaving the chest, moving to the
head, performing a head tiltchin lift maneuver to open the airway, taking in a breath,
bending over, getting a good mouth to mouth seal, blowing in the breath, rising up, taking
in a second breath, bending over again, recreating a good seal, blowing in the second
breath, watching the chest rise, leaving the head and returning to the chest, finding the
proper hand position, and finally beginning to compress the chest again! This kinesthetically complex set of tasks is much more difficult for the once trained, but unpracticed,
rescuer than is the rhythmic repetition of chest compression.
Hence in a practical, real-world setting, with a compression rate of 100 per minute (the
new value specified in the year 2000 international guidelines [2]), chest compressions
would be interrupted for ventilations a majority of the time (9 seconds for 15 compressions, 16 seconds for 2 ventilations). In this case chest compressions would be delivered
during only 36% of the total resuscitation time.
The consequences of interruptions of chest compressions for ventilation in adults have
recently been studied by the author and Karl B. Kern using mathematical modeling (70).
We developed equations describing oxygen delivery and blood flow during CPR as
functions of the number of compressions and the number of ventilations delivered over
time from principles of classical physiology. These equations were solved explicitly in
terms of the compression/ventilation ratio and evaluated for a wide range of conditions
using Monte Carlo simulations.
We found that as the compression to ventilation ratio is increased from 0 to 50 (that
is from 0:2 to 100:2) oxygen delivery to peripheral tissues increases to a maximum value
and then gradually declines. For parameters typical of standard CPR as taught and speci-

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Fig. 11. Oxygen delivery as a function of compression to ventilation ratio in the theoretical study
of Babbs and Kern (70). The compression to ventilation ratio is normalized to one ventilation.
Hence, a value of 20 represents 40:2, if two ventilations are given. Ideal professional rescuers are
assumed to deliver two rescue breaths in 5 seconds, as specified in guidelines. Lay rescuers are
assumed to deliver two breaths in 16 seconds, as observed in the field. Maximal oxygen delivery
occurs at ratios near 25:2 for ideal rescuers and 50:2 for lay rescuers.

fied in international guidelines (that is, 5 seconds to deliver two rescue breaths) maximum
oxygen delivery occurs at compression/ventilation ratios near 30:2. For parameters typical of actual lay rescuer performance in the field (that is, 16 seconds to deliver two rescue
breaths) maximum oxygen delivery occurs at compression to ventilation ratios near 60:2.
The complete curves are shown in Fig. 11. If these theoretical results are true in the real
world, current guidelines overestimate the need for ventilation during standard CPR by
two- to fourfold. In turn, blood flow and oxygen delivery to the periphery can be
improved by eliminating interruptions of chest compression for these unnecessary
ventilations.
Unnecessary interruptions of chest compression have actually become a greater problem with successive refinements of the guidelines. Historically, the problem was compounded when compression rate was increased from 60 per minute to 90 per minute, and
most recently in the year 2000, to 100 per minute. As shown in detail in reference (70),
the optimum ventilation to compression ratio for maximizing oxygen delivery to peripheral tissues is directly proportional to the compression rate. This means that if one
increases the rate of chest compression by a certain percentage, it is prudent to increase
the recommended compression to ventilation ratio by the same percentage also. For
example, suppose that 15:2 had been the optimum compression to ventilation ratio with
60 per minute compressions under the original CPR guidelines. Suppose further that the
guidelines changed to recommend a 120 per minute compression rate, just to keep the
arithmetic simple. Under the new guidelines, it would take exactly half the time to
deliver 15 compressions than it did previously, because the compression rate is doubled.

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The time for ventilations, however, would remain constant. Thus, the duration of interruptions of chest compression for ventilation must become a larger percentage of total
resuscitation time whenever the compression rate is increased without changing the
ventilation to compression ratio.
When the recommended compression rate was in fact increased from 60 per minute
to 90 per minute, the compression to ventilation ratio should have been automatically
increased from 15:2 to 23:2, simply by virtue of the fact that the compression rate had
increased. When the recommended compression rate was further increased to 100 per
minute, the compression to ventilation ratio should have been automatically increased
to 25:2. Actually 15:2 never was optimal for standard CPR in adults, but failure to
adjust ventilation as the compression rate was increased has further compounded the
problem.
The ultimate extension of the concept of increasing the number of chest compressions
between ventilation ventilations is continuous chest compression CPR without any
ventilations at all. Such a strategy, crazy as it may seem, has been extensively studied in
a swine model of resuscitation and has shown identical outcome results to standard 15:2
compression to ventilation CPR (68,11,12,71,72). Recently, Hallstrom et al. (73) have
reported a clinical study of simplified, dispatcher assisted CPR, in which no ventilations
are given. In this study, persons who called 911 for help with an adult, nontraumatic CA
and did not know CPR were coached by the 911 dispatcher to perform either traditional
CPR or compression-only CPR without any ventilations. The results of CPR without
ventilations were no worse than those of standard CPR. In particular, survival to hospital
discharge was greater among patients assigned to chest compression alone than among
those assigned to chest compression plus mouth-to-mouth ventilation (14.6 vs 10.4%,
using intention-to-treat analysis). There was no statistically significant difference in
favor of either standard CPR or chest compression-only CPR in this study of 303 randomized patients. Evidently, ventilation provided no added benefit. Importantly, Hallstroms
results were obtained for adult nontraumatic CA and are not necessarily indicative of
those that would be obtained in pediatric asphyxial arrest. This study highlights how little
we really know about the basic ABCs of CPR.

CONCLUSIONS
Principles of cardiovascular physiology tell us that during CA and CPR forward flow
of blood can be generated by external compression of the chest. Enough has been learned
in the last 25 years to suggest that most persons perform chest compressions suboptimally.
Much more emphasis needs to be placed on compression depth and technique rather than
on compression rate. Routine clinical monitors of effective chest compression need to be
developed and used widely. Still, the exact details of chest compression including such
fundamental variables as rate, duty cycle, amplitude, rescuer technique, and ventilation
to compression ratio remain suboptimal, under-investigated, and newly controversial
after all these years.
The original 1960s style CPR was developed on the basis of limited research and
educated guessworksome of it brilliant and insightful. The CPR pioneers like Kouwenhoven, Jude, Knickerbocker, Elam, Safar, and Redding had no government grants.
They were not supported by multinational drug companies. With limited resources, these
investigators made enormous progress. Nevertheless, the early standards for chest compression, which we have inherited today, were based on only partial understanding of the

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underlying physiology and biomechanics. Several plausible assumptions of the 1960s,

such as the mechanism of external cardiac massage and the required ventilation to perfusion ratio have proved to be oversimplifications in light of subsequent research.
Today at the dawn of the 21st century the topic of chest compression in CPR is ripe
for reassessment and renewed investigation. We need to know more about flow mechanisms with chest/abdominal compression and decompression. In order to optimize
CPR in children it would help to know about age related differences in chest size, chest
compliance, and CPR pump mechanisms. With more research we might discover
entirely new ways to apply force, create flow or raise coronary perfusion pressure. We
urgently need better sensorsbeyond ETCO2 and pulse-oxso that CPR on individuals
becomes less like flying a 747 without instruments and more like adjusting an anesthesia
machine or a mechanical ventilator. There need to be clinical evaluations of alternative
ventilation to compression ratios for lay CPR, and means of training individuals to
perform simpler, biomechanically easier, less complex series of steps with fewer interruptions of chest compressions. It is time for a renaissance of interest, research, and
teaching in the simple act of compressing the chest in CPR, which is, on closer inspection, anything but standard.

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