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From: Contemporary Cardiology: Cardiopulmonary Resuscitation Edited by: J. P. Ornato and M. A. Peberdy © Humana Press Inc., Totowa, NJ
C
ONTENTSI
NTRODUCTIONP
HYSIOLOGY OFC
HESTC
OMPRESSION INCPR T
ECHNIQUE OFC
HESTC
OMPRESSION INCPR
I
NTERRUPTION OFC
HESTC
OMPRESSIONS FORV
ENTILATIONC
ONCLUSIONSR
EFERENCESINTRODUCTION
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). Elimina- tion of the carotid artery pulse check in the year 2000 guidelines has abolished an unnec- essary 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 tech-
nique 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 pub-
lished (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 CPR—without
any ventilations—can be equally effective or more effective than standard CPR (6–12).
Even if one accepts that current guidelines describe correct chest compression tech- nique, several studies have shown that chest compressions are improperly performed by most lay rescuers and many health care workers as well (13–15).
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 mecha- nisms 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 Criley’s 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 pres- sure 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 (21–23). In this situ- ation, 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 predomi- nantly 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 (25–30). 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 (31–33), 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 compression–decompression 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 (38–42)
aims to improve priming of either chest pump through active abdominal counterpulsa-
tion. These methods have been called “CPR adjuncts,” because they usually require the
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 car- diac 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., “Ohm’s 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 compli- ances 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 (P
pump) 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 wave- forms and low systemic venous pressures. The data point representing the exact mini- mum, diastolic pressure at 82 mmHg is not plotted on the chart.
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.
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 pres- sures 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 (44–47), 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 rela-
tively recent concept in the physiology of CPR is the use of active decompression, rather
than simple relaxation, between chest compressions. Decompression can be accom-
plished 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
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.Fig. 3. Sketch of active compression–decompression cardiopulmonary resuscitation using a plunger-like device. Active decompression at a minimum ensures full chest wall recoil and pro- motes blood return to the chest.
approach is known as active compression–decompression 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 (47,52–54), which is sold commercially in Europe as the Ambu Cardiopump
®.
Figure 4 illustrates the steady-state effect of active decompression of the chest to nega- tive 20 mmHg, the maximum reported in the literature (52,55,56). This particular simula- tion 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 pres- sure phase, so that greater stroke output can be achieved on the next positive pressure phase.
Fig. 4. Pressures in a mathematical model of an adult human during cardiac arrest and active compression–decompression cardiopulmonary resuscitation with a pure cardiac pump mecha- nism. 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.
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 pro- motes 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. Oth- erwise, 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
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 “dias- tole,” 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.
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 compres- sion pressure is +60 mmHg. Maximal decompression pressure is –20 mmHg. Here forward flow is 1.1 L per minute and CPP is 22 mmHg.
Fig. 7. Relative forward flow in cardiopulmonary resuscitation (CPR) as a function of compres- sion 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 inches”—approx 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 (6–12 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 (x
0) 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 – x
0) if x > x
0for chest displacement, x, and constant, a.
However, if x < x
0CO = 0.
The mean value of x
0was 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 com-
pression. For chest compression depths greater than 2.5 cm relatively modest increases
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,
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.cries out for a more effective monitor of chest compression during CPR—either 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 effec- tive 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 esoph- ageal pressure rule provides a convenient yardstick for optimal chest compression. Unfor- tunately, 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 incorpo- rated into the chest compression pad of the Zoll AED-Plus automatic external defibril- lator. 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 physi- ologic end point, compression depth, accurately displayed to the rescuer on a push-by- push 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-
ably the same—reduced pump filling with shorter cycle times. When it comes to com- pression 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.
D
UTYC
YCLE ORC
OMPRESSIOND
URATIONIt 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 labo- ratory 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 electri- cally induced VF Fitzgerald et al. found inverted U-shaped functions at all rates (Fig. 10).
Peak flow occurred between 30 and 50 and duty cycle—that 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 observa- tion 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.
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.
Taylor’s 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. Increas- ing rate, assuming the compression duration is constant, automatically increases the duty cycle without requiring learns to alter two different aspects of their technique. Unfortu- nately 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.
H
ANDP
OSITION ON THEC
HESTProper 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 obstruct- ing 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 lacera- tion. If the compression point is shifted laterally the costochondral junctions may be subluxed or ribs may be broken.*
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.
*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.
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.
B
IOMECHANICS OFR
ESCUERA
CTIONAfter 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. Unfortu- nately, a fatigue-generating problem can easily occur during the recovery phase of res- cuer 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 L
EARNINGA
CTIVITY, P
ART1
To understand the importance of this point deeply, try standing up and bending for- ward 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 effective-
ness of active compression-decompression-CPR may simply be a result of its allowing
natural chest recoil to occur, rather than allowing the individual’s chest recoil to “rescue
the rescuer” from fatigue!
A L
EARNINGA
CTIVITY, P
ART2
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 thighs—the 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 individual—as close as possible—or 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 rescuer’s hips are lowered in the kneeling position with the back straight and firm, the weight of the rescuer’s body can be used to apply compression. As the rescuer’s hips are raised the quadriceps muscles of the anterior thigh can work to complete the cycle, although the rescuer’s 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 kneel- ing 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 3–5 minutes to avoid fatigue. As fatigue sets in, rescuers tend to revert to former habitual methods of chest compression, which are less effective.
A F
INALN
OTER
EGARDING THER
ELEASEP
HASEThe 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 consid- ered 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
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 defibrilla- tion is readily available.
INTERRUPTON OF CHEST COMPRESSIONS FOR VENTILATION
Current adult CPR by one or two rescuers is based on the traditional ABCs—airway,
breathing, circulation—with 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.
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 (62–64). More- over, 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 admin- ister 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 sys- temic perfusion below the value of approx 25 mmHg required for effective resuscitation (65–67).
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 indi- vidual, but the physical task of stopping compressions, leaving the chest, moving to the head, performing a head tilt–chin 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 kinestheti- cally 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 compres- sions, 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-
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 typi- cal 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 prob- lem with successive refinements of the guidelines. Historically, the problem was com- pounded 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 periph- eral 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.
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.
The time for ventilations, however, would remain constant. Thus, the duration of inter- ruptions 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 (6–8,11,12,71,72). 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 random- ized patients. Evidently, ventilation provided no added benefit. Importantly, Hallstrom’s 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 guesswork—some of it brilliant and insightful. The CPR pioneers like Kou- wenhoven, 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 com-
pression, which we have inherited today, were based on only partial understanding of the
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 inter- ruptions 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 inspec- tion, anything but “standard.”
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