Automatic and manual mechanical external chest compression devices for cardiopulmonary resuscitation

Resuscitation 47 (2000) 7 – 25 www.elsevier.com/locate/resuscitation

Review article

Automatic and manual mechanical external chest compression devices for cardiopulmonary resuscitation Lars Wik a,b,* a

Ulle6a˚l Uni6ersity Hospital, Institute for Experimental Medical Research, Kirke6n 166, N-0407 Oslo, Norway b The National Hospital of Norway, Medinno6a SF, 0027 Oslo, Norway Accepted 16 March 2000

Keywords: CPR; Mechanical CPR

1. Introduction Modern cardiopulmonary resuscitation (CPR) is only 35 years old [1], but Boehm did record successful external CPR in animals in 1878 [2], and Maass described the method in patients in 1892 [3]. Kouwenhoven rediscovered artificial circulation by manual external chest compressions (ECC) in 1960 with laboratory documentation and the first clinical proof of efficacy [1]. Later this group reported that external cardiac massage, combined with artificial respiration could restore cardiac and neurological function before defibrillation in more than 60% of their series of cardiac arrests [4]. Peter Safar organised the knowledge available in the early 1960s into ‘Airway, Breathing and Circulation’ [5]. ECC became step C of the US national [6] and World Federated Society for Anesthesiologists (WFSA) international guidelines [5]. These have been revised several times [7–10], and since 1992 the European Resuscitation Council have published European versions of the guidelines [11,12]. Early defibrillation is the most important single factor to influence survival in out-of-hospital resuscitation, but the majority of patients (\60%) * +47-22868495. E-mail address: [email protected] (L. Wik).

will receive basic life support consisting of chest compression and ventilation before defibrillation is available [12–15]. One study has even suggested that patients suffering cardiac arrest of more than 4 min should be given routinely chest compressions for a short period before defibrillation [16]. Scientists have tried to improve CPR techniques by focusing on manual or automatic driven devices to provide more consistent chest compressions and ventilations. At present there are manual and mechanical automatic devices that provide Vest CPR [17], active compression–decompression (ACD) CPR [18,19], phased thoracic–abdominal compression and decompression (PTACD) CPR [20], standard CPR [21–36], and automatic Belt CPR [unpublished data]. There are four main needs for mechanical ECC: 1. For the scientific study of CPR to provide consistent levels of support according to a protocol. 2. To optimise CPR performance based on the present standards for ECC. 3. To perform CPR using new protocols, optimised for machine resuscitation. 4. To provide basic life support (BLS), and allow the rescuer to concentrate on advanced life support (ALS) and start post resuscitative brain-oriented protective therapy.

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The purpose of the present article is to review the literature concerning clinical and laboratory use of external and non-invasive mechanical CPR devices. The reason why mechanical CPR is not widely adopted will also be discussed.

2. Chest compression Chest compression is a force, applied to the sternum or circumferentially around the chest. This force increases the pressure inside the thorax. Some advocate that this technique compresses the heart directly against the spine (heart pump theory) [1,37], others suggest that the force generates a diffuse pressure increase inside the chest (thoracic pump theory) [38]. Both theories postulate that blood is forced out of the chest during compression, and returns to the chest during the decompression phase through open valves due to passive generation of a negative pressure caused by the elastic recoil of the chest. During two-dimensional echocardiography it has been demonstrated that the mitral and aortic valves were open during the compression phase. The venus return to the right side of the heart occurred during the decompression phase. Compression of right ventricle and left atrium occurred to variable degree among the patients [38]. The authors concluded that stroke volume was not caused by direct compression of the right ventricle but by intrathoracic pressure fluctuations [38]. This conclusion is supported by Greene et al. [39] who demonstrated in humans that the mitral valve was open both during compression and decompression. The pulmonary valve opened partially during compression but more during decompression, the tricuspid valve never closed during compression but was open during decompression. The authors report that the left ventricular dimensions were more or less the same during CPR. It is hypothesised that antegrade flow during external chest compression is caused by a direct squeezing of the heart with more compression of the ventricles than the atria to generate a ventricular atrial pressure gradient that closes the atrioventricular valves. During passive decompression phase the ventricular pressure falls below the atrial pressure and hence the atrioventricular valves open to allow filling of the ventricles. This heart pump theory has been questioned by many.

Rudikoff et al. [40] showed that it was impossible to record a blood pressure in patients with a flail chest, when direct heart compression could be expected to be easier. In 1975 Criley observed a patient who had VF, started to cough rhythmically, and remained conscious [41]. The thoracic pump theory was thus introduced and later expanded by Halperin’s work on Vest CPR [17]. The idea of using a machine to perform rhythmical chest compressions on animals was first described by Pike et al. in 1908 [42]. The first mechanical CPR devices were manually or motor driven cardiac presses [21–24]. For the past 30 years automatic gas-powered chest compressors, and some electrically driven devices have been available [17,21–25,27–36,43–45]. Gas-powered machines use cylinders to provide the driving force. The devices are designed for installation on a patient trolley and are provided with a rigid back support to keep the patient in the correct position.

3. Device description Mechanical ECC devices may be divided into two main groups; automatic and non-automatic external chest compressors with or without a ventilation capacity. Gas or electricity powers the automatic devices and the non-automatic devices are driven by manpower (Table 1, Figs. 1–23).

3.1. Automatic mechanical ECC de6ices 3.1.1. The Thumper The Thumper (Fig. 1) is the best known device and has been used most in laboratory investigations of CPR. It consists of a vertical column attached to a baseplate. The baseplate is flat and does not assist head tilt. A cantilevered arm with a cylinder and piston assembly slides up and down on a column to adjust the piston position in relationship to the patient. Compressed gas (oxygen or air) drives the device. The built in ventilator is time-cycled and pressure limited. The device is useful inside hospital and in ambulances. 3.1.2. The Tra6enol HLR50 -90 The HLR (Fig. 2) discharges a fixed volume of gas, stored under relatively high pressure in a small container. The geometry and weight of the

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Table 1 An overview of automatic and manual mechanical external chest compression devices Automatic

Manual

Ventilator +

Ventilator −

Ventilator +

Ventilator −

(Fig. 1) Thumper gas powered (Fig. 2) Travenol/Baxter gas powered (Fig. 5) Beck–Rand electricity powered (Fig. 13) HLR Tamband gas powered (Fig. 14) Synchronised compression ventilation

(Fig. 3a) Heartsavaer 2000 E

(Fig. 19) Heart Reactivator Cardio Pulser

(Fig. 8) Cardiopump

–cardiopulmonary resuscitation gas powered (Fig. 15) Lifebelt E, Reanimator 3000G cardiopulmonary resuscitation, Lifesaver gas powered, Sirepuls 02G cardiopulmonary resuscitation, Suits gas powered (Fig. 22) Formenta Heart–Lung Machine

(Fig. 4) Iron Heart gas powered (Fig. 6) Vest cardiopulmonary resuscitation gas powered (Fig. 7) Hayek Oscillator gas powered (Fig. 16) Cardio Activator gas powered

(Fig. 9) Rentsch Cardiac Press (Fig. 10) Bowen Pulsator

(Fig. 17) Harkin Bramson electricity powered

(Fig. 20) Cardiopulmonary resuscitation Ass.Tool

(Fig. 18) ACD CPR

(Fig. 21) Knight Apparatus

(Fig. 11) Hepco Cardiac Massager (Fig. 12) Lifestick

(Fig. 23) Precordial balloon

unit make it easy to carry and use outside hospital. The unit uses four straps to hold the piston assembly on the chest. Adjustment of these straps is critical. Too low tension in the straps allows the piston to ‘wander’ on the chest. Excessive tension restricts chest expansion during ventilation, and prevents venous return to the chest during decompression. The applied plunger pressure can be varied but the rate is fixed to 60/min. Ventilation is achieved by intermittent flow of oxygen through a tube from the base of the appliance. This is delivered after every fifth chest compression via a non-rebreathing valve and mask. Ventilation pressure can be controlled.

3.1.3. Heartsa6er 2000 Heartsaver 2000 (Fig. 3a and b) is an electrically powered hydraulic device that can use an AC or DC power source. It is easily connected to an ambulance electrical system or mains power. It also has a built in battery that lasts 40 min for maximum compression force and rate. The device

consists of a wedge shaped board that supports a head tilt position. It has a ram with a plunger that travels 2–6 cm depending upon of the force used. A microprocessor controls the rate and force of compression, and can be programmed to provide

Fig. 1. Thumper gas powered.

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shoulders to each end of the ram. The design, shape and weight (8.3 kg) of the unit make it very portable. It can operate horizontally or vertically. It is therefore useful for chest compression in pregnant women, because the patient can remain in a lateral position. A suction head can easily replace the piston head providing the possibility of automatic mechanical compression and active decompression. The device does not have a ventilator.

Fig. 2. Travenol/Baxter gas powered.

Fig. 4. Iron Heart gas powered.

Fig. 3. (a) Heartsavaer 2000 E, (b) The aortapressure curve for mechanical and manual technique. Note the difference of compression spikes between the two methods indicated by arrows.

pauses after chest compressions. Both ends of the ram are connected to the board with a rod. The ram is stablised by straps, which run over the

Fig. 5. Beck – Rand electricity powered.

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operator can vary the pressure. Ventilation is performed manually by bag-valve-mask using spent oxygen from the plunger. The device is clumsy, heavy and not applicable for field conditions.

3.1.5. The Beck–Rand The Beck–Rand (Fig. 5) external cardiac compression device is a heavy (32 kg) portable battery powered unit. It produces rhythmic sternal pressure at fixed rates of 1 stroke per s with constant but adjustable force and depth of the compression. The device is not easily used in field conditions.

Fig. 6. Vest cardiopulmonary resuscitation gas powered.

3.1.4. The Iron Heart The Iron Heart (Fig. 4) consists of a plunger for chest compressions driven by compressed oxygen. The compression rate is fixed at 60/min and the

3.1.6. Vest CPR Vest CPR (Fig. 6) is a gas-powered device that fit the chest like a vest, and compresses the chest circumferentially as a unit. Since the whole chest is compressed it is not necessary to press as much as with standard chest compression. The force is spread over a larger area, which may prevent

Fig. 7. Hayek Oscillator gas powered.

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3.1.7. Reanimator 3000 Reanimator 3000 is a gas powered device that propels a piston. It stores the exhaust gas from chest compression in a flexible bag (test lung) for subsequent discharge into the lungs.

Fig. 10. Bowen Pulsator.

Fig. 8. Cardiopump.

Fig. 11. Hepco Cardiac Massager.

Fig. 9. Rentsch Cardiac Press.

trauma. An additional potential benefit of the circumferential vest is the ability to defibrillate the patient using electrodes placed in various locations on the vest itself. It may be difficult to use outside the hospital.

Fig. 12. Lifestick.

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3.1.8. Sirepuls O2 Sirepuls O2 is a pneumatic device driven by oxygen similar to the Thumper. 3.1.9. The Hayek Oscillator The Hayek Oscillator (Fig. 7) is based on moving air in and out of a stiff shell, which is placed around the thorax. By producing a positive and negative pressure in the cavity between the shell and the thorax the chest is compressed and actively decompressed respectively.

Fig. 13. HLR Tamband gas powered.

Fig. 15. Lifebelt E, Reanimator 3000G cardiopulmonary resuscitation, Lifesaver gas powered, Sirepuls 02G cardiopulmonary resuscitation, Suits gas powered.

Fig. 14. Synchronised compression ventilation–cardiopulmonary resuscitation gas powered.

Fig. 16. Cardio Activator gas powered.

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and weight of 1 kg. The handle is a circular disk with a cushioned surface for compression and an undercut suction grip for decompression. The ACD–CPR device incorporates a built-in monitor for both force and depth of compression and decompression to ensure chest compression similar to standard CPR and optimal decompression is provided.

3.2.2. The Rentsch Cardiac Press The Rentsch Cardiac Press (Fig. 9) consists of a flat baseplate that is placed under the patient and an inverted U-shaped frame that contains a sternal piston, an operating lever, and a linkage between the lever and the piston. Fig. 17. Harkin Bramson electricity powered.

3.2.3. The Bowen Pulsator The Bowen Pulsator (Fig. 10) uses a lever that is mounted on an arm, which adjusts on a vertical column attached to the baseplate.

Fig. 19. Heart Reactivator Cardio Pulser.

Fig. 18. ACD CPR.

3.2. Non-automatic ECC de6ices 3.2.1. The Cardiopump The Cardiopump is a device that provides active compression – decompression (ACD) CPR (Fig. 8). It consists of a rubber suction head, bellows, and handle, with a radius of 7 cm, height of 12 cm,

Fig. 20. cardiopulmonary resuscitation Ass.Tool.

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Fig. 21. Knight Apparatus.

3.2.4. Cardio Massager Cardio Massager (Fig. 11) consists of a baseplate, an upright, and a horizontal arm. A lever at the end of the horizontal arm is connected to a plunger, which delivers the sternal compression. The device is hand operated. 3.2.5. The Cardio Pulser The Cardio Pulser delivers compressions by a manual operated lever. A positive upward stroke of the lever works a piston, which delivers air through a tube to a mask and non-breathing valve. Each downstroke squeezes the heart and each upstroke ventilates the lungs. 3.2.6. The Lifestick (PTACD) Simultaneous sternal compression and abdominal decompression are alternated with simultaneous sternal decompression and abdominal compression using a manually powered cardiac assist device. The PTACD (Fig. 12) is constructed with a single rigid frame to which two disposable adhesive — backed pads are attached: one pad attaches to the sternum and the other to the abdomen. The rescuer applies alternating downward forces to the handles located on the sternal and abdominal portions of the device

4. Research To restart the heart, if initial defibrillation fails (or is not possible), coronary flow must be reinstated. Together with adequate myocardial blood flow or indicated, blood flow to the brain must be ensured during CPR to allow neurological as well as cardiovascular recovery [46–51]. With well performed CPR and the optimal use of epinephrine, brain blood flow reaches 30–60% of normal values, but myocardial blood flow is much more

limited, in the range of 5–20% of normal [44,52,53]. CPR research is designed to optimise these factors for successful resuscitation. This is done by using different CPR techniques generated manually or mechanically, by giving drugs, or by combining these factors. In most studies of CPR mechanical devices have been used to control one of the variables, namely chest compression. Mechanical ECC devices may also be used to optimise BLS and ALS. There are three studies of mechanical vs. manual CPR that support the statement that these units are valuable devices for BLS and ALS [18,27,28,30]. Several case reports [27,54–56] and one field study [31] support the conclusion that mechanical CPR equipment performing to manual standards can be a successful life support technique. The literature is scanty on studies comparing automatic mechanical ECC with manual and no studies have compared outcome with manual vs. mechanical standard CPR. Some studies have used automatic devices to control one variable (chest compression) during CPR in order to investigate how other different methods or treatment works during CPR.

4.1. Human use Taylor and colleagues [28] were among the first to use a mechanical instrument in studying CPR. They investigated the effectiveness of mechanical resuscitation by a pneumatic device (Thumper), and concluded that mechanical compressions appeared comparable with manual compressions when manual is performed under ‘ideal conditions’. This was an in-hospital study where patients were randomised within 10 min of starting CPR. Those given mechanical ECC were immediately placed on the pneumatic piston device but all had manual chest compressions first. Five patients

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out of 50 were discharged from hospital (three mechanical, two manual). The same group reported that a compression duration of 60% increased the antegrade arterial flow compared with a 50% duration [57]. Changing the compression rate at a duration of 60% had no substantial effect. They suggested that undue emphasis was placed on the precise rate rather than on duration

of chest compression. They also concluded that prolonged compression might increase forward flow during CPR [57]. They did not find any difference in 1-h survival or in the number of patients ultimately discharged from hospital. McDonald [27] studied the relationship of systolic arterial pressure (SAP) to mean arterial pressure (MAP), resulting from the use of mechanical

Fig. 22. Formenta Heart – Lung Machine.

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Fig. 23. Precordial balloon.

(Thumper) and manual ECC. He also studied the ability of mechanical and manual forms of chest compressions to produce such pressures in the same person. All 14 patients had CPR initiated outside hospital and all had failed to respond adequately to ALS at the scene or during transportation to hospital. Manual ECC resulted in a higher SAP in 13 of 14 cases. In 12 of the cases mechanical compressions resulted in an MAP that were greater or equivalent to the MAP generated by the manual method. This study showed that mechanical ECC was superior to manual ECC in generating a higher MAP. No patients were successfully resuscitated by either manual or mechanical CPR and arteriovenous pressure difference were not measured. Ornato et al. [29] showed that mechanical ECC provides consistent high quality chest compression and ventilation that does not vary with time. It also produces a higher MAP than manually performed CPR in humans. With mechanical ECC, tracheal intubation, defibrillation and central iv line insertion can be performed without interrupting ECC. The automatic chest compression devices remove the physical stress of performing CPR from the rescuer. ‘This allows fewer healthcare workers to do more for the patient in less time’ [29]. It allows the resuscitation team leader to focus on the intellectual challenge of determining the cause of arrest, restarting the heart and establishing effective spontaneous circulation. The Thumper causes less physical injury to the chest and internal organs than manually performed CPR [29]. Some investigators have used mechanical devices to show the benefits of monitoring end tidal CO2 during CPR [35,58,59]. During CPR end

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tidal CO2 provides information about the adequacy of ventilation and perfusion. If ventilation is held constant by using a ventilator that is synchronised with ECC and CO2 production is assumed constant, a change in the end tidal CO2 concentration should reflect a change in systemic and pulmonary blood flow. If CO2 is inadequately delivered to the lungs, it cannot be eliminated. Consequently end tidal CO2 will be very low, indicating low blood flow generated by the chest compression. Steedman and Robertson used the Thumper to determine the patterns of arterial and central venous blood gas measurements in 27 patients undergoing CPR in an accident and emergency department [60]. The mean difference between central venous PCO2 (Pcv) and arterial PCO2 (Pa) ranged from 5.18 to 5.83 kPa reflecting the low blood flow in patients undergoing CPR. They speculated that the large arterial/central venous differences in PCO2 was due to the poor cardiac output achieved during CPR. But these differences were less than those achieved during standard manual CPR in a comparable group of pre-hospital cardiac arrest patients treated in USA (mean Pcv −Pa CO2 =60.5 mmHg) [61]. Based on this, Steedman and Robertson suggest that the mechanical device is more efficient than manual technique. Ornato et al. [62] showed by using the Thumper that there is a direct linear relationship between the applied chest compression force and the resultant arterial pressure and blood flow. This was measured by end tidal CO2 concentration. Manually, these high forces are very difficult to deliver over a longer time, because of fatigue. Dickinson et al. showed in human that end tidal CO2 was either increased or was stable during mechanical chest compression compared to a decrease in eight out of ten patients or no difference in the remaining two of the manual group. They concluded that (significant differences between the two groups) mechanical chest compressions appears to be superior to standard manual chest compression as measured by end tidal CO2 in maintaining cardiac output during ACLS resuscitation of out-of-hospital cardiac arrest patients [18]. Simulated CPR with H-L-R 50-90, 1–2 h post mortem showed that minimal functions were possible to achieve, and it was possible to get very

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good blood gases, but it was not better than manual CPR [63]. Manual ECC often has to be interrupted when performed in- or outside hospital, and during transportation to hospital [19]. Sefrin [31] monitored intravascular arterial blood pressure recordings for both manual and mechanical ECC. The blood pressure in the mechanical ECC group was continuously stable, compared with the unstable and intermittent blood pressure in the manual group. Sefrin [31] also used the H-L-R device in a doctor manned ambulance, and concluded that the device was a useful adjunct to standard equipment and frees the doctor to initiate additional therapeutic measured or treatment. Drouven [30] has reported 72 resuscitation attempts with Sirepuls O2, 12.5% of the patients were discharged from hospital. The average CPR time before ROSC was 41 min. Most of the patients had myocardial infarction and cardiac failure with life threatening cardiac arrhythmia and pulmonary embolism. In pulmonary embolism an early use of Sirepuls O2 seems to be promising because of reports about a mechanical fragmentation of the thrombus during CPR [63]. This is supported in this study. Drouven also point out that the ventilation pause of Sirepuls O2 secures an effective respiration. In conclusion mechanical CPR provides efficient circulation and ventilation over a long period of time. In humans Halperin et al. [17] documented that Vest CPR increased CPP and aortic pressure compared to standard manual CPR. They also found a trend toward a greater likelihood of the return of spontaneous circulation with Vest CPR than with continued manual CPR. Smithline et al. [43] used the biphasic extrathoracic pressure method performed by the Hayek Oscillator in a human study and documented that the method significantly increased CPP when compared with mechanical (Thumper) CPR (CPP: − 1.29 8.6 vs. 6.2 9 6.9 mmHg). Additionally they found a trend towards improved systemic perfusion as indicated by the improved venous to atrial PCO2 gradient. During circulatory failure the venous to arterial PCO2 gradient increases due to increased transit time across systemic and pulmonary capillary beds. This primarily leads to an increase in venous PCO2 and to a lesser degree to a fall in arterial PCO2. Improvement in this gradient would reflect a reduction in capillary transit time

and thus improved systemic circulation. They also concluded that oxygenation and ventilation appeared to be adequate without delivering positive pressure ventilation with its associated risks. Manual ACD–CPR has been used in human cardiac arrests and has generated improved haemodynamics [mean diastolic filling time (61%) [64], transmitral valve velocity time integral (82– 140%) [64–66], and left ventricular stroke volume (85%) [66], compared to standard CPR. Recently several studies have documented better outcome with ACD if the rescuers are well trained and practised [67], but other studies have not found any improved outcome [68]. Kvalsvik et al. [36] have used the new Heartsaver 2000 in human resuscitation provided by the Norwegian Air-ambulance. He concludes that the device improves quality of prolonged CPR, with high user satisfaction, and much easier and more flexible in use compared with previous machines.

4.2. Animal use Mechanical ECC devices are the most important tools in CPR research. By using a machine for ECC and ventilation it is possible to control two of the important variables during CPR. Different types of treatment, ventilation or chest compression techniques can be tested in the same controlled and standardised model. One of the early mechanised units was designed for programmable CPR intended to investigate the optimisation of CPR protocol. The experiments were conducted and reported by Birch et al. [69]. These animal studies used baboons, one pig, and several dogs. The authors concluded that the overall effectiveness of mechanical closed chest cardiac compression was impressive without any further specification. With the knowledge Taylor et al. [28,57] had from human research they designed a new study on dogs with their modified Thumper. The new device delivered chest compressions with a variable rate and duration of 60% synchronously with ventilations providing airway pressures of 70–100 cmH2O. This approach, which they called new CPR (NCPR) was compared with CPR at a rate of 60/min, and a compression duration of 50% in arrested dogs. They found that NCPR augmented carotid flow without compromising oxygenation.

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Controversy exists regarding both the physiological mechanisms responsible for systemic blood flow during CPR and the technique that generates the best circulatory support. Newton et al. [70] studied physiological comparisons of different external cardiac massage techniques on dogs. They compared five external chest compression techniques based on electromagnetic flow probes in the ascending and descending aorta while matched micromanometers measured aortic, left ventricular, and pleural pressures. They concluded that high-impulse manual compression provided the highest coronary perfusion pressure and was superior to other groups both statistically and physiologically in generating hemodynamics. In a canine model, Kern et al. [33] could not find a significant difference between manual and mechanical external chest compressions during CPR. Endpoints were hemodynamics produced during CPR, resuscitation success at 30 min, 24-h survival, neurologic function of survivors and CPR produced trauma. Ten animals in each group underwent 20 min of VF, during which CPR was performed for 17 min. Hemodynamics produced with manual and mechanical chest compressions were similar, and seven of ten animals in each group were resuscitated. Halperin et al. [71] tried to determine the blood flow to vital organs during CPR in dogs. They also tried to show whether blood flow during CPR results from intrathoracic pressure fluctuations or direct cardiac compressions. Blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range, but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, flow should be dependent on the compression rate and force, but above a certain threshold, insensitive to compression duration. The study provided confirmation that the major mechanism for blood flow during manual CPR in large dogs is manipulation of intrathoracic pressure. Vital organ flow was unchanged when rate was increased from 60–150/min, but is markedly enhanced when the duration of each compression is increased from 15 to 45%. This duration dependence but rate insensitivity is diametrically opposed to the influence of changes in compression duration and rate on the hemodynamics of direct cardiac compression. In this study Vest CPR produced perfusion pressures and flow

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similar to those produced by conventional external chest compression. Vest CPR increases the intrathoracic pressure without significant sternal displacement. In another study Rabson et al. [72] showed that an intrathoracic pressure of 30–60 mmHg and carotid flows of 20–60 ml/min could be generated by Vest CPR in dogs. Angelos et al. [73–75] used a Thumper on dogs to show that the coronary perfusion pressure generated by mechanical ECC benefited neurologic outcome at 96 h after VF no flow 10 min and then 5 min CPR–BLS followed by another 5 min CPR–ALS. Wik et al. [34] used the Heartsaver 2000 during 30 min of ECC on dogs. They compared the use of Heartsaver 2000 with optimal performed manual ECC. All animals in both groups (n=6× 2) were easily defibrillated and achieved ROSC after 30 min of ECC. They all regained consciousness and were neurologically normal after 4 h. Differences between the groups were found in all hemodynamics and end tidal CO2 in favour of mechanical ECC. The study also documented differences in how aortic pressure tracings was generated (Fig. 3b). Mechanical ECC also produced better peripheral circulation and fewer traumas. They concluded that this mechanical ECC device might be used instead of manual ECC. Mechanical ACD–CPR has been used to investigate the optimal performance of the ACD technique in respect of rate [76], duty cycle [77], level of decompression [78], and to standardise the performance [44,45,76–78].

5. Discussion The potential advantages of manual ECC are: simplicity, immediate availability, adaptability to field conditions, no need for extra equipment and always have available. But there are some disadvantages: it is variably performed, the operator can tire quickly. The technique is also stressful, difficult during transportation, and can only be performed with the patient in the supine position. Usually EEC is undertaken with the chest compressed manually by applying the hands with significant force (up to 686 N (70 kp)) in short-lasting pushes with a frequency of approximately 100 compressions per min. Since ECC and ventilation has to be delivered each minute according to the

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ratio of chest compression and ventilation, ECC must be paused during ventilation of an non-intubated patient. It is possible to deduce a mathematical formula, which calculates the number of chest compressions and ventilation delivered per minute, based on different variables (Fig. 24). Such a mathematically based steering system may be built in to operate automatically driven devices. Mechanical devices must provide as many of these manual features as possible. Most of the effort to develop mechanised equipment has been aimed at optimising standard CPR performance. In the future equipment must also aim to solve more of the measures, which are necessary to perform during CPR. It is necessary to develop equipment that can free the hands of the rescuer from ECC and ventilation. The devices must be portable, light, and easy to operate and assemble, a single unit and be able to fit on a stretcher. Then the rescuer can concentrate on the ‘art of resuscitation’. The rescuer can lead the resuscitation and administer drugs and defibrillate while ECC and ventilation continues. Simultaneously they can start prevention of post/peri-resuscitation brain damage (post resuscitation syndrome). This ‘brain oriented’ intensive therapy may be started at the scene. Prehospital cardiac arrest studies have reported hospital discharge rates from 2 to 33% [79]. The low likelihood of survival after resuscitative efforts outside the hospital is a result of several factors. Some are related to fate, such as the patient’s

Fig. 24. Equation to calculate the number of actually delivered chest compressions and ventilations. f, compression working frequency; nc, compression per cycle, nv, ventilations per cycle; Tc, time for one cycle; Nc, cycles per minute; VT, tidal volume (l); MV, minute ventilation; c, compression; 6, ventilation; TOT, total; n, number.

cardiac rhythm or whether or not the collapse was witnessed, and if bystanders started good qualitatively CPR [80]. Others are related to the emergency medical response itself, such as the response interval from the collapse to the beginning of CPR and defibrillation [79] and how fast they are able to deliver the different aspects of ACLS [81]. The limiting factor will in some cases be the number and skills of personnel, and in others the availability of defibrillators. We may speculate that mechanical CPR may influence these factors in a positive way. It is well known that CPR skill and performance varies among health care workers inside and outside hospital. Sometimes it is even impossible to do CPR manually. This is well documented during ambulance transport [19,82], and it is easy to understand how difficult it is on a stretcher. Fatigue is another important issue. Hightower et al. [83] investigated the influence of fatigue on CPR quality over time on manikins. Professional CPR nurses performed manual standard CPR for 5 min and were instructed to indicate when they tired. The study demonstrated that objectively measured by a Skillmeter manikin they tired after 1–2 min and performed worse quality CPR. But subjectively it took 4–5 min for them to indicate that the quality was worse. Thus CPR was performed suboptimally and in an unrecognised fashion for 3 min. By contrast mechanical CPR remains qualitatively close to 100% both at the site and during transport, and is not influenced by time [19]. How this will influence outcome is not known. Many prehospital studies have investigated drugs or techniques that might improve outcome after cardiac arrest based on positive results from animal tests. But these effects have not been demonstrated in humans. Animal studies are performed on healthy animals, and chest compression and ventilation are performed optimally by manual or automatic techniques. We may never be able to control the most important factor for outcome in humans, the underlying disease. However, we may be able to deliver the best quality external chest compression by using automatic mechanical resuscitators and thereby provide optimal blood flow to the brain and heart in order to improve potential therapeutic effects. Mechanical ECC cannot replace for defibrillation. On the contrary it is an essential adjunct. Patients who do not respond to the first defibrilla-

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tion need chest compression in order to circulate oxygenated blood to the myocardium and brain. We also may give epinephrine and sometimes buffers. Mechanical ECC allows all these factors to occur while maximum and consistent flow is delivered and therefore achieve a greater number of successful defibrillations, and discharges from hospital. At present about 30% of patients with an initial rhythm of VF achieve ROSC. We also know that about 30% of the patients that have cardiac arrest have VF as their first ECG verified rhythm. Therefore the majority of cardiac arrest patients need ECC before defibrillation. Optimally performed CPR may increase the number of patients with ROSC and subsequently the number of patients discharged from hospital. This effect of automatic mechanical external chest compression devices has yet to be shown in human studies. Mechanised CPR can secure a stable CPR process according to the standards and guidelines for CPR [19,34]. If recommendations change it is easy to change the settings for mechanised CPR devices appropriately. The potential advantages will be even greater during transport and during prolonged CPR. Pinchak et al. [84] compared CPR expert/non experts with mechanical CPR. They concluded that mechanical CPR was more consistent than manual expert/non expert CPR. The chest compression depth was greater with the experts compared to both non-experts and mechanical. They concluded that a greater compression and decompression acceleration was necessary to maintain a hold phase, and peak compression acceleration during mechanical CPR is usually two to five times greater than during the manual technique. It is known that CPR in hypothermic patients, and in certain intoxication or poisoning cases may have to be continued for several hours before they respond to treatment [54]. Both in hypothermia and intoxication mechanical ECC is indicated. Cardiopulmonary bypass (CPB) may be the best, but it is not available in all hospitals. Mechanical ECC may also be used as a bridge to CPB, open-heart surgery, or organ perfusion until donation/transplantation is possible. In these cases mechanical ECC can secure organ perfusion until more sophisticated support is available. Cardiac arrest in late pregnancy occurs once in 30 000 pregnancies [85] and survival is exceptional [86] unless it occurs during general anaesthesia.

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Postural vena cava occlusion and the supine hypotensive syndrome in late pregnancy were first described in 1953 by Howard et al. [87]. The syndrome is due to the uterus compressing the vena cava in the supine position. Lees et al. [88] showed that this resulted in decreased right atrial pressure, decreased cardiac output, and reflex increased systemic vascular resistance. Kasten et al. [89] demonstrated in a dog model that the reduction in venous return and subsequent effect on cardiac output, regional perfusion and pharmacokinetics are important determinants of the ability to resuscitate dogs given toxic doses of bupivacaine intravenously. Should an accidental intravenous administration of the drug occur in late pregnancy and result in cardiovascular collapse, resuscitation must include displacement of the uterus away from the vena cava. There are three ways to do this. One is emergency caesarean section, another is pushing the uterus laterally, and the last is to do lateral decubitus CPR. The device most suitable for this must be a device where the patient is strapped to the device. In other words, the device must work without piston displacement when the patient is in the left oblique or left lateral decubitus position. It is impossible to do manual ECC with the patient in lateral decubitus. This may be possible with some of the mechanical devices, but it will take a long time to apply it and the possibility of piston displacement is great. One of the devices (Heartsaver 2000) has solved some of these problems. It is applied to the patient as a backpack. It is possible that the same hemodynamic disturbances seen during CPR on a pregnant women may also occur in resuscitation attempts in extremely obese people. Maybe these patients should be resuscitated in lateral decubitus position. However, I am not aware of any study investigating the possible positive effect of resuscitation an obese cardiac arrest patient in this position. The interposed abdominal counterpulsation (IAC) technique [90] needs manpower, and may therefore benefit from mechanical ECC. By combining this technique with active decompression [91] bloodflow may be improved. Sterz et al. have reported results of manual performance of the combination of ACD and IAC [20]. Together these techniques may be so complicated that an automatic machine is required.

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Only 20 – 35% of normal resting cardiac output is achieved with ECC. Any reduction in the quality of ECC, as inevitably occurs with operator fatigue or variations in technique will transform an already marginal level of circulation to one that cannot support life. The brain will receive insufficient oxygen and irreversible cell injury will ensue. Therefore there are theoretical advantages of mechanical over manual ECC. The efficacy of the mechanical devices over the manual technique has not yet been demonstrated in clinical studies, and therefore a study is needed where their potential advantages in usage and effects on outcome may be documented. To have more patients discharged from hospital the following goals must be attained: (1) Train and retrain CPR the whole population. (2) Defibrillators in all ambulances and greater public access defibrillators. (3) If studies with mechanical ECC devices indicate improved survival they should be used in ambulances and hospitals. We must also be aware of the fact that more patients will be transported to hospital if the use of automatic mechanical CPR devices becomes widespread. This may mean that a greater number of potentially salvageable brains and hearts are brought to the hospital. Hospitals must be prepared to take care of these patients in a way that outcome will be improved. This means more aggressive attempts to restart the heart with drugs, defibrillation, open chest CPR, and cardiopulmonary bypass [92,93] with acute heart surgery when indicated. Automatic mechanical CPR can then be used as a bridge to advanced life support because CPR can be continued for a long time [94,95].

6. Conclusion Most of the devices that have been available have operational limitations due to application time, they are cumbersome to install and operate, they are unstable on the chest, and heavy and expensive to purchase. Therefore, there are few human studies that reveal any differences between manual and mechanical external chest compressions with respect to haemodynamics and outcome. At present time there are no data showing improved survival with mechanical ECC devices simply because these studies have yet not been

performed. Automatic mechanical CPR is however well documented to deliver adequate circulation to the brain and heart during CPR. Mechanised equipment will never replace the manual first aid techniques. The goal must be to provide mechanised equipment that is easy to apply and use on the patient as early as possible. The device must also produce a haemodynamic profile better or at least as good as optimally performed manual ECC [34]. Then it may be possible to increase the probability of a good outcome because the machine will cope with the ABC aspect of BLS while the rescuer can concentrate on ALS interventions without interruption of ECC.

Acknowledgements Special thanks to Colin Robertson for important input.

References [1] Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed chest cardiac massage. J Am Med Assoc 1960;173:1064– 7. [2] Boehm R. Uber Wiederbelebung nach Vergiftungen und Asphyxia. Arch Exp Pathol Pharmakol 1878;8:68–101. [3] Maass. Die Methode der Wiederbelebung bei Herztod nach Chloroformeinathmung. Berlin Klin Wochschr 1892;29:265 – 8. [4] Jude JR, Kouwenhoven WB, Knickerbocker GG. Cardiac arrest: report of application of external cardiac massage in 118 patients. J Am Med Assoc 1961;178:1063– 70. [5] Safar P, Bircher N. In: Stavanger A, Laerdal WB, editors. Cardiopulmonary Cerebral Resuscitation, 3rd ed. Saunders, 1988. [6] American Heart Association (AHA) and National Academy of Sciences – National Research Council (NAS – NRC). Standards for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiac Care (ECC). J Am Med Assoc 1966;198:372 – 9. [7] American Heart Association (AHA) and National Academy of Sciences – National Research Council (NAS – NRC). Standards for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiac Care (ECC). J Am Med Assoc 1974;227(Suppl):833– 66. [8] American Heart Association (AHA) and National Academy of Sciences – National Research Council (NAS – NRC). Standards for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiac Care (ECC). J Am Med Assoc 1980;244(Suppl):453– 509.

L. Wik / Resuscitation 47 (2000) 7–25

[9] American Heart Association (AHA) 1985 National Conference. Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). J Am Med Assoc 1986;255(Suppl):2905–84. [10] American Heart Association. Guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). J Am Med Assoc 1992;268:2171–302. [11] European Resuscitation Council. Guidelines for basic and advanced life support. Resuscitation 1992;24:103 – 22. [12] European Resuscitation Council. European Resuscitation Council Guidelines for Resuscitation. Amsterdam: Elsevier, 1998. [13] Pepe P. Advanced cardiac life support: state of the art. In: Vincent JL, editor. Emergency and Intensive Care. Berlin: Springer, 1990:565–85. [14] Eisenberg MS. Who shall live? Who shall die? In: Eisenberg MS, Bergner L, Hallstrom AP, editors. Sudden Cardiac Death in the Community. Philadelphia, PA: Praeger, 1984:44–58. [15] Callaham M, Braun O, Valentine W, Clark DM, Zegans C. Prehospital cardiac arrest treated by urban first responders: profile of patient response and prediction of outcome by ventricular fibrillation waveform. Ann Emerg Med 1993;22:1664–77. [16] Cobb LA, Fahrenbruch CE, Walsh TR, Copass MK, Olsufka M, Breskin M, Hallstrom AP. Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation. J Am Med Assoc 1999;281:1182–8. [17] Halperin HR, Tsitlik JE, Gelfand M, Weisfeldt ML, Gruben KG, Levin HR, Rayburn BK, Chandra NC, Scott CJ, Kreps BJ, Siu CO, Guerci AD. A preliminary study of cardiopulmonary resuscitation by circumferential compressions of the chest with use of a pneumatic vest. New Engl J Med 1993;329:762–8. [18] Dickinson ET, Verdile VP, Schneider RM, Saluzzo RF. Effectiveness of mechanical versus manual chest compressions in out-of-hospital cardiac arrest resuscitation: a pilot study. Am J Emerg Med 1998;16:289–92. [19] Sunde K, Wik L, Steen PA. Quality of mechanical, manual standard and active compression–decompression CPR on the arrest site and during transport in a manikin model. Resuscitation 1997;34:235–42. [20] Sterz F, Behringer W, Berclanovich A, Wernigg H, Domanowits H, Muellner M, Schreiber W, Ohley WJ, Schoerkhuber W, Laggner AN. Active compression – decompression of thorax and abdomen (Lifestick™ — CPR) in patients with cardiac arrest. Circulation 1996;94:I-9 abstract. [21] Pearson JW, Navarro RN, Redding JS. Evaluation of mechanical devices for closed chest cardiac massage. Anesth Analg 1966;45:590–8. [22] Harkins GA, Bramson ML. Mechanical external cardiac massage for cardiac arrest and for support of failing heart. J Sci Res 1961;1:197–200. [23] Safar P, Harris LC. The Beck-Rand External Cardiac Compression Machine. Anesthesiology 1963;24:586 – 8. [24] Nachlas MM, Siedband MP. A simple portable pneumatic pump for external cardiac massage. Am J Cardiol 1962;10:107–90.

23

[25] Nachlas MM, Siedband MP. Clinical experiences with mechanical cardiac massage. Am J Cardiol 1965;15:310– 9. [26] Knight ICS. New apparatus for intermittent cardiac compression. Br Med J 1964;1:894. [27] McDonald JL. Systolic and mean arterial pressures during manual and mechanical CPR in humans. Ann Emerg Med 1982;11:292 – 5. [28] Taylor GJ, Rubin R, Tucker M, Greene HL, Rudikoff MT, Weisfeldt ML. External Cardiac compression: a randomized comparison of mechanical and manual techniques. J Am Med Assoc 1978;240:644 – 6. [29] Ornato JP. Clinical and research experience with the Michigan Instruments CPR Thumper. Medical College of Virginia, 1989 Letter. [30] Drouven F, Reininghaus A, Schaar H, et al. LudwigBoltzmann Symposium: Cardiopulmonary and Cerebral Reanimation. Mechanical versus Manual CPR. Academic Teaching Hospital of RWTH Aachen, 1986. [31] Sefrin P. Verbesserungen bei Wiederbelebungsversuchen im Notarztwagen (Improvements with reanimation attempts in clinobiles). Erfahrungen mit einem Wiederbelebungsgerat (Experiences with a mechanical resuscitator). Med Klin 1973;68:211 – 5. [32] Hempelmann G, Hartmann W, Gille J. Untersuchung zur Reanimation mit einem Herz- Lungen-Rettungsgerat (Report about reanimation with a cardiac-pulmonary life saving apparatus). Intensivmed 1974;11:155 –64. [33] Kern B, Carter AB, Showen RL, et al. Manual versus mechanical cardiopulmonary resuscitation in an experimental canine model. Crit Care Med 1985;13:899–903. [34] Wik L, Bircher NG, Safar P. A comparison of prolonged manual and mechanical external chest compression after cardiac arrest in dogs. Resuscitation 1996;32(3):241– 50. [35] Ward KR, Menegazzi JJ, Zelenak RR, Sullivan RJ, McSwain NE. A comparison of chest compressions between mechanical and manual CPR by monitoring endtidal PCO2 during human cardiac arrest. Ann Emerg Med 1993;22:669 – 74. [36] Kvalsvik O, Siljehaug HO, Vaagenes P, Gisvold SE. External cardiac compressions (ECC) with a new portable automatic device. A feasibility study. Acta Anesthesiol Scand 1991;35(Suppl 96):194 abstract. [37] Maier GW, Tyson GS, Olsen CO, et al. The physiology of external cardiac massage: high impulse cardiopulmonary resuscitation. Circulation 1984;70:86 – 101. [38] Rich S, Wix HL, Shapiro EP. Clinical assessment of heart chamber size and valve motion during cardiopulmonary resuscitation by two-dimensional echocardiography. Am Heart J 1981;102:368 – 73. [39] Greene HL, Janko CL, Cobb LA. Visualisation of cardiac valve motion in man during external chest compression using two-dimensional echocardiography. Implications regarding the mechanism of blood flow. Circulation 1981;63:1417 – 21. [40] Rudikoff MT, Maughan WL, Effron M, Freund P, Weisfeldt ML. Mechanisms of blood flow during cardiopulmonary resuscitation. Circulation 1980;61:345–52. [41] Criley JM, Blaufuss AH, Kissel GL. Cough-induced cardiac compression. Self-administered from of car-

24

[42]

[43]

[44]

[45]

[46]

[47]

[48] [49] [50]

[51] [52]

[53]

[54]

[55]

[56] [57]

[58]

[59]

L. Wik / Resuscitation 47 (2000) 7–25

diopulmonary resuscitation. J Am Med Assoc 1976;236:1246–50. Pike FH, Guthrie CC, Stewart GN. Studies in resuscitation. 1. The general conditions affecting resuscitation of blood and the heart. J Exp Med 1908;10:371–418. Smithline HA, Rivers EP, Rady MY, Blake HC, Noevak RM. Biphasic extrathoracic pressure CPR. A human pilot study. Chest 1994;105:842–6. Lindner KH, Pfenninger EG, Schurman W, Lurie KG, Schurmann W, Lindner IM, Ahnefeld FW. Effects of active compression–decompression resuscitation on myocardial and cerebral blood flow in pigs. Circulation 1993;88:1254–63. Wenzel V, Fuerst RS, Idris AH, Banner MJ, Rush WJ, Orban DJ. Automatic mechanical device to standardize active compression–decompression CPR. Ann Emerg Med 1995;25:386–9. Safar P. Resuscitation from clinical death: pathophysiologic limits and therapeutic potensials. Crit Care Med 1988;16:923–41. Bircher N, Safar P. Cerebral preservation during cardiopulmonary resuscitation. Crit Care Med 1985;13:185–90. Siesjo BK. Mechanisms of ischemic brain damage. Crit Care Med 1988;16:854–963. Safar P. Cerebral resuscitation after cardiac arrest: a review. Circulation 1986;74(Suppl IV):138–53. Bircher NG. Cardiopulmonary–cerebral resuscitation: brain resuscitation, mediators, glucose and anesthetics. Anaesthesiology 1990;3:259–64. Safar P, Bircher NG. Cardiopulmonary–Cerebral Resuscitation, 3rd ed. Philadelphia, PA: Saunders, 1988. Brown CG, Werman HA, Davis EA, Hobson J, Hamlin RL. The effects of graded doses of epinephrine on regional myocardial blood flow during cardiopulmonary resuscitation in swine. Circulation 1987;75:491–7. Sharff JA, Pantley G, Noel E. Effects of time on regional organ perfusion during two methods of cardiopulmonary resuscitation. Ann Emerg Med 1984;13:649–55. Gomez-Arnau J, Criado A, Martinez MV, Aguilar MG, Avello F. Hyperkalemic cardiac arrest: prolonged heart massage and simultaneoues hemodialysis. Crit Care Med 1981;9:556–7. Lilja GP, Hill M, Ruiz E, Clinton J. Clinical assessment of patients undergoing CPR in the emergency department. JACEP 1979;8:81–3. Sims JK, Penick M. How much CPR is enough CPR? JACEP 1978;7:218–20 letter. Taylor GJ, Tucker WM, Greene HL, Rudikoff MT, Weisfeldt ML. Importance of prolonged compression duration during cardiopulmonary resuscitation in man. New Engl J Med 1977;296:1515–7. Sanders AB, Ewy GA, Bragg S, Atlas M, Kern KB. Expired PCO2 as a prognostic indicator of successful resuscitation from cardiac arrest. Ann Emerg Med 1985;14:948–52. Garnett AR, Ornato JP, Gonzalez ER, et al. The clinical value of end tidal carbon dioxide monitoring during cardiopulmonary resuscitation. J Am Med Assoc 1987;257:512–5.

[60] Steedman DJ, Robertson CE. Acid base changes in arterial and central venous blood during cardiopulmonary resuscitation. Arch Emerg Med 1992;9:169–76. [61] Grundler W, Weil MH, Rackow EC. Arterial venous carbon dioxide and Ph gradients during cardiac arrest. Circulation 1986;74:1071 – 4. [62] Ornato JP, Levine RL, Young DS, et al. The effect of applied chest compression on systemic arterial pressure and end tidal carbon dioxide concentration during CPR in human beings. Ann Emerg Med 1989;18:732 –7. [63] Ko¨hle W, Nechwatal W, Strauch M, Rasche H. Hochdosierte Streptokinasetherapie bei fulminanter Lungenarterienembolie. Vhdl Dt Ges Inn Med 1983;89:517. [64] Cohen TJ, Tucker KJ, Lurie KG, Redberg RF, Dutton JP, Dwyer KA, Chin MC, Gelb AM, Scheinman MM, Schiller NB, Callaham ML. Active compression –decompression resuscitation: a new method of cardiopulmonary resuscitation. J Am Med Assoc 1992;267:2916– 23. [65] Cohen TJ, Tucker KJ, Redberg RF, Lurie KG, Chin MC, Dutton JP, Scheinman MM, Schiller NB, Callaham ML. Active compression – decompression resuscitation: a novel method of cardiopulmonary resuscitation. Am Heart J 1992;124:1145– 50. [66] Tucker KJ, Cohen TJ, Redberg RF, Schiller NB, Callaham MED. Active compression decompression resuscitation: analysis of transmitral flow and left ventricular volume by transesophageal echocardiography in humans. J Am Coll Cardiol 1993;22:1485 – 93. [67] Plaisance P, Lurie KG, Vicaut E, Adnet F, Petit J-L, Epain D, Ecollan P, Gruat R, Cavagna P, Biens J, Payen D, Cantineau J-P, Gizzi M, Ferracci C, Leopold C, Giroud M, Hennequin E, Lapandry C, Magne P, Prudhomme C, Lambert Y. A comparison of standard cardiopulmonary resuscitation and active compression– decompression resuscitation for out-of-hospital cardiac arrest. New Engl J Med 1999;341:569 – 75. [68] Wik L, Mauer D, Robertson C. The first European pre-hospital active compression – decompression (ACD) cardiopulmonary resuscitation workshop: a report and a review of ACD – CPR. Resuscitation 1995;30:191–202. [69] Birch LH, Kenney LJ, Doornbos F, et al. A study of external cardiac compression. J Mich Med Soc 1962;61:1346. [70] Newton JR, Glower DD, Wolfe JA. A physiologic comparison of external cardiac massage techniques. J Thorac Cardiovasc Surg 1988;95:892 – 901. [71] Halperin HR, Tsitlik JE, Guerci AD, et al. Determinants of blood flow to vital organs during cardiopulmonary resuscitation in dogs. Circulation 1986;73:539 – 50. [72] Rabson J, Goldberg H, Bromberger-Barnea B, Permutt S. The use of a pneumatic vest to generate carotid flow in a canine model of circulatory arrest. Circulation 1987;59 – 60(Suppl II):768 abstract. [73] Angelos M, Safar P, Reich H. External cardiopulmonary resuscitation preserves brain viability after prolonged cardiac arrest in dogs. Am J Emerg Med 1991;9:436 – 43. [74] Angelos M, Safar P, Reich H. A comparison of cardiopulmonary resuscitation with cardiopulmonary by-

L. Wik / Resuscitation 47 (2000) 7–25

[75]

[76]

[77]

[78]

[79]

[80]

[81]

[82] [83]

[84]

pass after prolonged cardiac arrest in dogs. Reperfusion pressures and neurologic recovery. Resuscitation 1991;21:121–35. Angelos M, Reich H, Safar P. Factors influencing variable outcomes after ventricular fibrillation cardiac arrest of 15 minutes in dogs. Resuscitation 1990;20:57– 66. Sunde K, Wik L, Naess PA, Grund F, Nicolaysen G, Steen PA. Improved haemodynamics with increased compression–decompression rates during ACD–CPR in pigs. Resuscitation 1998;39:197–205. Sunde K, Wik L, Naess PA, Ilebekk A, Nicolaysen G, Steen PA. Effect of different compression–decompression cycles on haemodynamics during ACD–CPR in pigs. Resuscitation 1998;36:123–31. Wik L, Naess PA, Ilebekk A, Nicolaysen G, Steen PA. Effects of various degrees of compression and active decompression on haemodynamics, end-tidal CO2, and ventilation during cardiopulmonary resuscitation of pigs. Resuscitation 1996;31:45–57. Eisenberg MS, Horwood BT, Cummins RO, ReynoldsHaertle R, Hearne TR. Cardiac arrest and resuscitation: a tale of 29 cities. Ann Emerg Med 1990;19:179– 86. Wik L, Bircher NG, Steen PA. Quality of bystander cardiopulmonary resuscitation influences outcome after prehospital cardiac arrest. Resuscitation 1994;28:195 – 203. Wik L, Steen PA. The ventilation/compression ratio influences the effectiveness of two rescuer advanced cardiac life support on a manikin. Resuscitation 1996;31:113–9. Stapleton ER. Comparing CPR during ambulance transport. J Emerg Med Serv 1991;September:63–72. Hightower D, Thomas SH, Stone CK, Dunn K, March JA. Decay in quality of closed-chest compressions over time. Ann Emerg Med 1995;26:300–3. Pinchak AC, Hancock DE, Hagen JF, Hall FB. Chest wall acceleration and force measurements in simulated manual and mechanical cardiopulmonary resuscitation. Crit Care Med 1988;16:151–60.

.

25

[85] Rees GAD, Willis BA. Resuscitation in late pregnancy. Anaesthesia 1988;43:347 – 9. [86] Stokes IM, Evans J, Stone M. Myocardial infarction and cardiac arrest in the second trimester followed by assisted vaginal delivery under epidural analgesia at 38 weeks gestation. Br J Obstet Gynaecol 1984;91:197–8 Case report. [87] Howard BK, Goodson JH, Mengert WF. Supine hypotensive syndrome in late pregnancy. Obstet Gynecol 1953;1:371 – 7. [88] Lees MM, Scott DB, Kerr MG, Taylor SH. The circulatory effects of recumbent postural change in late pregnancy. Clin Sci 1967;32:453 – 65. [89] Kasten GW, Martin ST. Resuscitation from bupivacaine-induced cardiovascular toxicity during partial inferior vena cava occlusion. Anesth Analg 1986;65:341–4. [90] Sack JF, Kesselbrenner MB, Bregman D. Survival from in-hospital cardiac arrest with interposed abdominal counterpulsation during cardiopulmonary resuscitation. J Am Med Assoc 1992;3:379 – 85. [91] Cohen TJ, Tucker KJ, Lurie KG, Redberg RF, Dutton JP, Dwyer KA, Schwab TM, Chin MC, Gelb AM, Scheinman MM, Schiller NB, Callaham ML. Active compression – decompression. A new method of cardiopulmonary resuscitation. J Am Med Assoc 1992;21:2916 – 23. [92] Safar P, Abramson N, Angelos M, et al. Emergency cardiopulmonary bypass for resuscitation from prolonged cardiac arrest. Am J Emerg Med 1990;8:55–67. [93] Reich H, Angelos M, Safar P, et al. Cardiac resusciability with cardiopulmonary bypass after increasing ventricular fibrillation times in dogs. Ann Emerg Med 1990;19:887 – 90. [94] Stept WJ, Safar P. Cardiac resuscitation following two hours of cardiac massage and 42 countershocks. Anesthesiology 1966;27:97 – 100. [95] Cleveland JC. Complete recovery after cardiac arrest for three hours. New Engl J Med 1971;284:334 – 5.