Hemodynamic mechanisms in CPR: a theoretical rationale for resuscitative thoracotomy in non-traumatic cardiac arrest

Experimental work over the past decade has revealed three distinct mechanisms for generating artificial circulation during cardiac arrest and resuscitation. To isolate these mechanisms and study them in pure form, and in particular to characterize circulation during open vs. closed chest cardiopulmonary resuscitation (CPR), we developed an electrical model of the human circulatory system. Heart and blood vessels were modeled as resistive-capacitive networks, pressures in the chest, abdomen, and vascular compartments as voltages, blood flow as electric current, blood inertia as inductance, and the cardiac and venous valves as diodes. External pressurization of thoracic and abdominal vessels, as would occur in CPR, was simulated by application of half-sinusoidal voltage pulses. Simulations included two modes of creating artificial circulation: the cardiac pump mechanism, in which the atria and ventricles of the model were pressurized simultaneously, as occurs during open chest cardiac massage, and the thoracic pump mechanism, in which all intrathoracic elements of the model were pressurized simultaneously, as is likely to occur in closed chest CPR. The two mechanisms were compared for the same peak applied pressure (80 mmHg). Pure cardiac pump CPR generated near normal systemic perfusion pressures throughout the compression cycle. Pure thoracic pump CPR generated much lower systemic perfusion pressure only during the diastolic phase of the compression cycle. Simulation of cardiac compression at rates from 40 to 100/min produced total flows of 2500-3300, myocardial flows of 150-250 and cranial flows of 600-800 ml/min, depending on the compression rate. In contrast, thoracic pump CPR produced a total flow of approx. 1200, myocardial flow of 70, and cranial flow of 450 ml/min, independently of the compression rate. Direct cardiac compression is an inherently superior hemodynamic mechanism, because it can generate greater perfusion pressure throughout the compression cycle. If one presumes that improved blood flow during CPR is the key to more successful resuscitation, then it is reasonable to conclude that direct heart massage is the most effective available way to achieve this end.     

Theoretically Optimal Duty Cycles for Chest and Abdominal Compression during External Cardiopulmonary Resuscitation

Objective: To use an electronic model of human circulation to compare the hemodynamic effects of different durations of chest compression during external CPR, both with and without interposed abdominal compression (IAC).
Methods: An electrical analog model of human circulation was studied on digital computer workstations using SPICE, a general-purpose circuit simulation program. In the model the heart and blood vessels were represented as resistive-capacitive networks, pressures as voltages, blood flow as electric current, blood inertia as inductance, and cardiac and venous valves as diodes. External pressurization of the heart and great vessels, as would occur in IAC-CPR, was simulated by the alternate application of damped rectangular voltage pulses, first between intrathoracic vascular capacitances and ground, and then between intra-abdominal vascular capacitances and ground. With this model compression frequencies of 60, 80, and 100 cycles/min and duty cycles ranging from 10% to 90%, both with and without IAC, were compared.
Results: There was little difference in hemodynamics when the overall compression frequency was varied between 60 and 100 cycles/min, but the effects of duty cycle were substantial. During both standard CPR and IAC-CPR, total flow and coronary flow were greatest at chest compression durations equal to 30% of cycle time. Interposed abdominal compression substantially improved simulated systemic blood flow and perfusion pressure at all duty cycles, compared with standard CPR without abdominal compression. Mean arterial pressure > 75 mm Hg and artificial cardiac output > 2.0 L/min could be generated by 30% duty cycle compression with IAC. Coronary perfusion in the model is clearly optimized at 30% chest compression (i.e., high-impulse chest compression technique).
Conclusion: Combined high-impulse chest compressions and IACs maximize blood flow during CPR in the electrical analog model of human circulation.     

Relative effectiveness of interposed abdominal compression CPR: sensitivity analysis and recommended compression rates

Interposed abdominal compression, IAC-CPR incorporates alternating chest and abdominal compressions to generate enhanced artificial circulation during cardiac arrest. The technique has been generally successful in improving blood flow and survival compared to standard CPR; however, some questions remain. OBJECTIVE: To determine "why does IAC-CPR produce more apparent benefit in some subjects than in others?" and "what is the proper compression rate, given that there are actually two compressions (chest and abdomen) in each cycle?" METHOD: Computer models provide a means to search for subtle effects in complex systems. The present study employs a validated 12-compartment mathematical model of the human circulation to explore the effects upon systemic perfusion pressure of changes in 35 different variables, including vascular resistances, vascular compliances, and rescuer technique. CPR with and without IAC was modeled. RESULTS AND CONCLUSIONS: Computed results show that the effect of 100 mmHg abdominal compressions on systemic perfusion pressure is relatively constant (about 16 mmHg augmentation). However, the effect of chest compression depends strongly upon chest compression frequency and technique. When chest compression is less effective, as is often true in adults, the addition of IAC produces relatively dramatic augmentation (e.g. from 24 to 40 mmHg). When chest compression is more effective, the apparent augmentation with IAC is relatively less (e.g. from 60 to 76 mmHg). The optimal frequency for uninterrupted IAC-CPR is near 50 complete cycles/min with very little change in efficacy over 20-100 cycles/min. In theory, the modest increase in systemic perfusion pressure produced by IAC can make up in part for poor or ineffective chest compressions in CPR. IAC appears relatively less effective in circumstances when chest pump output is high.     

Simultaneous sternothoracic cardiopulmonary resuscitation: a new method of cardiopulmonary resuscitation

No existing device for cardiopulmonary resuscitation (CPR) is designed to exploit both the "cardiac pump" and the "thoracic pump" effect simultaneously. The purpose of this study was to measure the haemodynamic effect of a new simultaneous sternothoracic cardiopulmonary resuscitation (SST-CPR) device that could compress the sternum and constrict the thoracic cavity simultaneously in a canine cardiac arrest model. After 4 min of ventricular fibrillation, 24 mongrel dogs were randomized to receive standard CPR (n=12) or SST-CPR (n=12). SST-CPR generated a new pattern of the aortic pressure curve presumed to be the result of both sternal compression and thoracic constriction. SST-CPR resulted in significantly higher mean arterial pressure than standard CPR (68.9+/-16.1 vs. 30.5+/-10.0 mmHg, P<0.01). SST-CPR generated higher coronary perfusion pressure than standard CPR (47.0+/-11.4 vs. 17.3+/-8.9 mmHg, P<0.01). End tidal CO(2) tension was also higher during SST-CPR than standard CPR (11.6+/-6.1 vs. 2.17+/-3.3 mmHg, P<0.01). In this preliminary animal model study, simultaneous sternothoracic cardiopulmonary resuscitation generated better haemodynamic effects than standard, closed chest cardiopulmonary resuscitation.     

Improved hemodynamic performance with a novel chest compression device during treatment of in-hospital cardiac arrest

INTRODUCTION: The purpose of this pilot clinical study was to determine if a novel chest compression device would improve hemodynamics when compared to manual chest compression during cardiopulmonary resuscitation (CPR) in humans. The device is an automated self-adjusting electromechanical chest compressor based on AutoPulse technology (Revivant Corporation) that uses a load distributing compression band (A-CPR) to compress the anterior chest. METHODS: A total of 31 sequential subjects with in-hospital sudden cardiac arrest were screened with institutional review board approval. All subjects had received prior treatment for cardiac disease and most had co-morbidities. Subjects were included following 10 min of failed standard advanced life support (ALS) protocol. Fluid-filled catheters were advanced into the thoracic aorta and the right atrium and placement was confirmed by pressure waveforms and chest radiograph. The coronary perfusion pressure (CPP) was measured as the difference between the aortic and right atrial pressure during the chest compression's decompressed state. Following 10 min of failed ALS and catheter placement, subjects received alternating manual and A-CPR chest compressions for 90 s each. Chest compressions were administered without ventilation pauses at 100 compressions/min for manual CPR and 60 compressions/min for A-CPR. All subjects were intubated and ventilated by bag-valve at 12 breaths/min between compressions. Epinephrine (adrenaline) (1mg i.v. bolus) was given at the request of the attending physician at 3-5 min intervals. Usable pressure signals were present in 16 patients (68 +/- 6 years, 5 female), and data are reported from those patients only. A-CPR chest compressions increased peak aortic pressure when compared to manual chest compression (153 +/- 28 mmHg versus 115 +/- 42 mmHg, P < 0.0001, mean +/- S.D.). Similarly, A-CPR increased peak right atrial pressure when compared to manual chest compression (129 +/- 32 mmHg versus 83 +/- 40 mmHg, P < 0.0001). Furthermore, A-CPR increased CPP over manual chest compression (20 +/- 12 mmHg versus 15 +/- 11 mmHg, P < 0.015). Manual chest compressions were of consistent high quality (51 +/- 20 kg) and in all cases met or exceeded American Heart Association guidelines for depth of compression. CONCLUSION: Previous research has shown that increased CPP is correlated to increased coronary blood flow and increased rates of restored native circulation from sudden cardiac arrest. The A-CPR system using AutoPulse technology demonstrated increased coronary perfusion pressure over manual chest compression during CPR in this terminally ill patient population.     

Revisiting the cardiac versus thoracic pump mechanism during cardiopulmonary resuscitation

The mechanism of forward blood flow due to external chest compressions during cardiopulmonary resuscitation (CPR) remains controversial, with the main theories being based on either a cardiac, or thoracic pump mechanism. Both potential mechanisms are well investigated by echocardiographic assessment. In the present case, a postoperative complication of cardiac tamponade that was detected by a thoracoabdominal CT-scan, led to cardiac arrest with subsequent successful CPR over 15 min until definitive surgical management was performed. This observation suggests that the thoracic pump mechanism may have been the predominant mechanism of forward blood flow in the present case of a pericardial tamponade.     

Increased cortical cerebral blood flow with LUCAS; a new device for mechanical chest compressions compared to standard external compressions during experimental cardiopulmonary resuscitation

OBJECTIVE: LUCAS is a new device for mechanical compression and decompression of the chest during cardiopulmonary resuscitation (CPR). The aim of this study was to compare the efficacy of this new device with standard manual external chest compressions using cerebral cortical blood flow, cerebral oxygen extraction, and end-tidal CO2 for indirect measurement of cardiac output. Drug therapy, with adrenaline (epinephrine) was eliminated in order to evaluate the effects of chest compressions alone. METHODS: Ventricular fibrillation (VF) was induced in 14 anaesthetized pigs. After 8 min non-intervention interval, the animals were randomized into two groups. One group received external chest compressions using a new mechanical device, LUCAS. The other group received standard manual external chest compressions. The compression rate was 100 min(-1) and mechanical ventilation was resumed with 100% oxygen during CPR in both groups. No adrenaline was given. After 15 min of CPR, external defibrillatory shocks were applied to achieve restoration of spontaneous circulation (ROSC). Cortical cerebral blood flow was measured continuously using Laser-Doppler flowmetry. End-tidal CO2 was measured using mainstream capnography. RESULTS: During CPR, the cortical cerebral blood flow was significantly higher in the group treated with LUCAS (p = 0.041). There was no difference in oxygen extraction between the groups. End-tidal CO2, an indirect measurement of the achieved cardiac output during CPR, was significantly higher in the group treated with the LUCAS device (p = 0.009). Restoration of spontaneous circulation was achieved in two animals, one from each group. CONCLUSIONS: Chest compressions with the LUCAS device during experimental cardiopulmonary resuscitation resulted in higher cerebral blood flow and cardiac output than standard manual external chest compressions. These results strongly support prospective randomised studies in patients to evaluate this new device.     

Performance of chest compressions by laypersons during the Public Access Defibrillation Trial

Background

Increasing evidence indicates that health professionals often may not achieve guideline standards for cardiopulmonary resuscitation (CPR). Little is known about layperson CPR performance.

Methods

The investigation was a retrospective cohort study of cardiac arrest patients treated by layperson CPR and one model of automated external defibrillator (AED) as part of the Public Access Defibrillation Trial (n = 26). CPR was measured using software that integrates the event log, ECG signal, and thoracic impedance signal. We assessed chest compression fraction (proportion of attempted resuscitation spent performing chest compressions), prompted compression fraction (proportion of attempted resuscitation spent performing compressions during AED-prompted periods), compression rate, and compressions per minute.

Results

Of the 26 cases, 13 presented with ventricular fibrillation and 13 with nonshockable rhythms. Overall, during the period when patients did not have spontaneous circulation, the median chest compression fraction was 34% (IQR 17-48%), median prompted chest compression fraction was 49% (IQR 30-66%), and the median chest compression rate was 96/min (IQR 90-110/min). Taken together, the median chest compression delivered per minute among all arrests was 29 (IQR 20-42). CPR characteristics differed according to initial rhythm: median chest compression per minute was 20 (IQR 13-29) among ventricular fibrillation and 42 (IQR 28-47) among nonshockable rhythms (p = 0.003).

Conclusions

In this study of trained laypersons, CPR varied substantially and often did not achieve guideline parameters. The findings suggest a need to improve CPR training, consider changes to CPR protocols, and/or improve the AED-rescuer interface.     

The influence of nonlinear intra-thoracic vascular behaviour and compression characteristics on cardiac output during CPR

Clinical observations suggest that the assumption of a linear relationship between chest compression pressure and cardiac output may be oversimplified. More complex behaviour may occur when the transmural pressure is large, changing the compliances and resistances in the intra-thoracic vasculature. A fundamental understanding of these compression induced phenomena is required for improving CPR.An extensively used, lumped element computer model (model I) of the circulation was upgraded and refined to include the intrathoracic vasculature (model II). After validation, model II was extended by adding variable compliances and resistances (model III) to the vascular structures. Successively, ranges of compression pressures, frequencies, duty cycles and compression pulse shapes were applied while controlling all other parameters. Cardiac output was then compared.The nonlinearities in compliance and resistance become important, limiting factors in cardiac output, starting in our experimental series at 70 mmHg peak compression pressure, and increasing with higher pressures. This effect is reproducible for sinusoidal and trapezoidal compression forms, resulting in lower cardiac output in all experiments at high compression pressures. Duty cycle and wait time are key parameters for cardiac output.Our data strongly indicate that vascular compliance, especially the ability of vessels to collapse (and potentially the cardiac chambers), can be a central factor in the limited output generated by chest compressions. Just pushing ‘harder’ or ‘faster’ is not always better, as an ‘optimal’ force and frequency may exist. Overly forceful compression can limit blood flow by restricting filling or depleting volume in the cardiac chambers and central great vessels.     

Theoretical effects of fluid infusions during cardiopulmonary resuscitation as demonstrated in a computer model of the circulation

Recent studies have shown the potential adverse effects of venous volume loading on blood flow during closed chest cardiopulmonary resuscitation (CPR). To examine the effect of arterial and venous infusions, we employed a published computer simulation of the circulation during CPR. This model uses computer simulated electrical networks to model the heart and great vessels. CPR was modeled with compressions at a rate of 80/min and a force of 80 mmHg. Fluid infusions, simulated as current pulses into the abdominal aorta and superior vena cava, were given to measure their effect on myocardial and cranial blood flow. With 600 ml/min infusions into the abdominal aorta, there was a 12% peak increase in myocardial flow and a 3.8% peak increase in cranial flow. Every 100 ml/min increase in infusion from 0 to 900 ml/min produced a 1.4 ml/min linear increase in myocardial flow and a 4.2 ml/min linear increase in cranial flow. In agreement with previous CPR model studies, simulated vasoconstriction of abdominal and lower extremity vessels resulted in increased myocardial and cranial flows. As resistance of these vessels was increased, abdominal aortic infusions resulted in greater flow augmentations. In contrast to arterial results, infusions at 600 ml/min into the vena cava resulted in a 2.2% decrease in myocardial flow and a 0.62% decrease in cranial flow. Rise and fall times for initiation and cessation of flow augmentations were equal to four compression cycles. We conclude that these findings demonstrate the theoretical benefits of rapid arterial infusions during CPR with increases in myocardial and cranial blood flow. This method may provide an early temporary adjunct to myocardial perfusion during CPR.     

Depth of sternal compression and intra-arterial blood pressure during CPR in infants following cardiac surgery

The optimal depth of sternal compressions during cardiopulmonary resuscitation (CPR) in infants is unknown; current guidelines recommend compressing to a depth of 1/3rd to 1/2 the anterior-posterior (AP) diameter of the chest. Our experience to compress the chest at 1/3rd the AP diameter often fails to provide an adequate blood pressure response. We reviewed our experience with CPR, depth of compressions, and arterial blood pressure response in a cohort of 6 infants having cardiac surgery and subsequent cardiac arrest. Pediatric advanced life support measures were initiated, with attempted compressions to 1/3rd the AP chest diameter. Depth of attempted compressions was increased to approximately 1/2 the AP chest diameter if systolic BP response was inadequate (i.e., <60 mm Hg systolic). BP tracings were reviewed and contiguous recordings were evaluated as compressions were attempted at 1/3rd and 1/2 the AP chest diameter. The age range was from 2 weeks to 7.3 months, and median age was of 1.0 month. The mean systolic BP was 83.4 mm Hg for the 1/2 AP chest diameter technique vs. 51.6 mm Hg for the 1/3rd AP diameter approach, p < 0.001. The mean diastolic pressure was similar with both strategies (30.5 vs. 30.6 mm Hg, p = 0.99). In this cohort of 6 infants having cardiac surgery and subsequent cardiac arrest, attempting to compress the chest at 1/2 the AP diameter increased systolic blood pressure by 62% compared to attempting to compress 1/3rd the AP diameter. Perhaps resuscitators should attempt to compress infants’ chests 1/2 rather than 1/3rd the AP diameter of the chest.     

Resuscitation,Prolonged Cardiac Arrest,and an Automated Chest Compression Device

Background: The European Resuscitation Council's 2005 guidelines for cardiopulmonary resuscitation (CPR) emphasize the delivery of uninterrupted chest compressions of adequate depth during cardiac arrest. Objectives: To describe how the circumstances of out-of-hospital cardiac arrest can impede the performance of CPR, and how this situation can be overcome. Case Report: The presentation of two cases of prolonged CPR (48 min and 120 min, respectively) with an automated chest compression device, the AutoPulse^®, under difficult circumstances. Both patients survived without neurological sequelae. Conclusion: Prolonged chest compressions may be necessary in some cardiac arrests. These cases suggest that automated chest compression devices may increase the chance of a favorable outcome in these rare situations.     

Chest Compression and Ventilation Rates during Cardiopulmonary Resuscitation: The Effects of Audible Tone Guidance

Objectives: To determine: 1) whether chest compressions during CPR are being performed according to American Heart Association (AHA) guidelines during cardiac arrest; and 2) the effect of an audio prompt to guide chest compressions on compliance with AHA guidelines and hemodynamic parameters associated with successful resuscitation. Methods: An observational clinical report and laboratory study was conducted. A research observer responded to a convenience sample of cardiac arrests within a 300-bed hospital and counted the rate of chest compressions and ventilations during CPR. To evaluate the effect of an audio prompt on CPR, health care providers performed chest compression without guidance using a porcine cardiac arrest model for 1 minute, followed by a second minute in which audio guidance was added. Chest compression rates, arterial and venous blood pressures, end-tidal CO₂ (ETCO₂) levels, and coronary perfusion pressures were measured and compared for the two periods. Results: Twelve in-hospital cardiac arrests were observed in the clinical part of the study. Only two of 12 patients had chest compressions performed within AHA guidelines. No patient had respirations performed within AHA guidelines. In the laboratory, 41 volunteers were tested, with 66% performing chest compressions outside the AHA standards for compression rate without audible tone guidance. With guided chest compressions, the mean (± SD) chest compression rate increased from 74 ± 22 to 100 ± 3/min (p < 0.01). End-tidal CO₂ levels increased from 15 ± 7 to 17 ± 7 torr (p < 0.01). Coronary perfusion pressure increased minimally with audible tone-guided chest compressions. Conclusions: The majority of Basic Cardiac Life Support-certified health care professionals did not perform CPR according to AHA-recommended guidelines. The use of audible tones to guide chest compression resulted in significantly higher chest compression rates and ETCO₂ levels.     

Does a more “physiological” infant manikin design effect chest compression quality and create a potential for thoracic over-compression during simulated infant CPR?

Poor survivability following infant cardiac arrest has been attributed to poor quality chest compressions. Current infant CPR manikins, used to teach and revise chest compression technique, appear to limit maximum compression depths (CDmax) to 40 mm. This study evaluates the effect of a more “physiological” CDmax on chest compression quality and assesses whether proposed injury risk thresholds are exceeded by thoracic over-compression.     

Subcapsular liver haematoma after cardiopulmonary resuscitation by untrained personnel

Although early cardiopulmonary resuscitation (CPR) is associated with increased survival of sudden cardiac arrest victims, it may also result in miscellaneous injuries. A 25-year-old inebriated man rescued from drowning in a swimming pool was apnoeic and pulseless after being pulled out of the water. Successful CPR was provided by untrained bystanders, including abdominal thrusts thought to remove water from the airways and chest compressions to provide haemodynamic support. As the patient progressively improved during his subsequent hospital stay, he complained of right upper abdominal and thoracic pain. A computed tomographic scan showed a 11 cm subcapsular haematoma contiguous to the right hepatic lobe. A favourable outcome was obtained after conservative, non-operative treatment. Subcapsular haematoma of the liver is a potentially life threatening complication that warrants consideration in survivors of cardiac arrest who have received closed chest compression and/or abdominal thrusts.     

Does the compression to ventilation ratio affect the quality of CPR: a simulation study.

Experience has shown that better quality CPR leads to a greater chance of a patient surviving a cardiac arrest. Simple CPR techniques, such as using only chest compressions, lead to better skill retention and greater willingness to attempt resuscitation on strangers. However, it is not clear from clinical or experimental studies whether such techniques offer any physiological benefit over more usual 5:1 or 15:2 compression:ventilation ratios. Computer simulations of blood flow and gas exchange during CPR showed that continuous chest compressions produced much greater blood flow (1.39 l/min) than 5:1 (0.73 l/min), 15:2 (0.86 l/min) or 50:5 (0.94 l/min) ratios. However, the ratio of 5:1 produced the highest arterial oxygen levels, with continuous chest compressions the lowest. The most appropriate measure of CPR efficiency appears to be the amount of oxygen delivered to the body during CPR. The ratios of 15:2 and 50:5 produced significantly greater oxygen delivery to the body than 5:1, the greater blood flow with these techniques offsetting the slightly lower arterial oxygen levels. The best oxygen delivery was provided by continuous chest compression in the early stages of CPR. After 3-4 min however, hypoxia meant that continuous compressions became worse than the other techniques. Spontaneous gasping by the patient during CPR was able to extend the effectiveness of chest compression only CPR for much longer.     

Design of near-optimal waveforms for chest and abdominal compression and decompression in CPR using computer-simulated evolution

OBJECTIVE: To discover design principles underlying the optimal waveforms for external chest and abdominal compression and decompression during cardiac arrest and cardiopulmonary resuscitation (CPR). METHOD: A 14-compartment mathematical model of the human cardiopulmonary system is used to test successive generations of randomly mutated external compression waveforms during cardiac arrest and resuscitation. Mutated waveforms that produced superior mean perfusion pressure became parents for the next generation. Selection was based upon either systemic perfusion pressure (SPP = thoracic aortic minus right atrial pressure) or upon coronary perfusion pressure (CPP = thoracic aortic pressure minus myocardial wall pressure). After simulations of 64,414 individual CPR episodes, 40 highly evolved waveforms were characterized in terms of frequency, duty cycle, and phase. A simple, practical compression technique was then designed by combining evolved features with a constant rate of 80 min(-1) and duty cycle of 50%. RESULTS: All ultimate surviving waveforms included reciprocal compression and decompression of the chest and the abdomen to the maximum allowable extent. The evolved waveforms produced 1.5-3 times the mean perfusion pressure of standard CPR and greater perfusion pressure than other forms of modified CPR reported heretofore, including active compression-decompression (ACD)+ITV and interposed abdominal compression (IAC)-CPR. When SPP was maximized by evolution, the chest compression/abdominal decompression phase was near 70% of cycle time. When CPP was maximized, the abdominal compression/chest decompression phase was near 30% of cycle time. Near-maximal SPP/CPP of 60/21 mmHg (forward flow 3.8 L/min) occurred at a compromise compression frequency of 80 min(-1) and duty cycle for chest compression of 50%. CONCLUSIONS: Optimized waveforms for thoraco-abdominal compression and decompression include previously discovered features of active decompression and interposed abdominal compression. These waveforms can be used by manual (Lifestick-like) and mechanical (vest-like) devices to achieve short periods of near normal blood perfusion non-invasively during cardiac arrest.     

Cardiopulmonary resuscitation for cardiac arrest: the importance of uninterrupted chest compressions in cardiac arrest resuscitation

Over the last decade, the importance of delivering high-quality cardiopulmonary resuscitation (CPR) for cardiac arrest patients has become increasingly emphasized. Many experts are in agreement concerning the appropriate compression rate, depth, and amount of chest recoil necessary for high-quality CPR. In addition to these factors, there is a growing body of evidence supporting continuous or uninterrupted chest compressions as an equally important aspect of high-quality CPR. An innovative resuscitation protocol, called cardiocerebral resuscitation, emphasizes uninterrupted chest compressions and has been associated with superior rates of survival when compared with traditional CPR with standard advanced life support. Interruptions in chest compressions during CPR can negatively impact outcome in cardiac arrest; these interruptions occur for a range of reasons, including pulse determinations, cardiac rhythm analysis, electrical defibrillation, airway management, and vascular access. In addition to comparing cardiocerebral resuscitation to CPR, this review article also discusses possibilities to reduce interruptions in chest compressions without sacrificing the benefit of these interventions.     

A new device producing manual sternal compression with thoracic constraint for cardiopulmonary resuscitation

OBJECTIVE: Blood flow during conventional cardiopulmonary resuscitation (CPR) is usually less than adequate to sustain vital organ perfusion. A new chest compression device (LifeBelt) which compresses both the sternum and the lateral thoraces (compression and thoracic constraint) has been developed. The device is light weight, portable, manually powered and mechanically advantaged to minimize user fatigue. The purpose of this study was to evaluate the mechanism of blood flow with the device, determine the optimal compression force and compare the device to standard manual CPR in a swine arrest model. METHODS: Following anesthesia and instrumentation, intravascular contrast injections were performed in four animals and the performance characteristics of the device were evaluated in eight animals. In a comparative outcome study, 42 anesthetized and instrumented swine were randomized to receive LifeBelt or manual CPR. Ventricular fibrillation (VF) was induced electrically and was untreated for 7.5 min. After 7.5 min, countershocks were administered and chest compressions initiated. Pulseless electrical activity (PEA) was observed after one to three shocks in all animals. CPR was continued until restoration of spontaneous circulation (ROSC) or for 10 min after the first shock. If ROSC had not occurred within 5 min of beginning CPR, 0.01 mg/kg of epinephrine (adrenaline) was administered. During CPR, peak systolic aortic pressure (Ao), diastolic coronary perfusion pressure (CPP-diastolic aortic minus diastolic right pressure) and end-tidal CO(2) were measured. RESULTS: Angiographic studies demonstrated cardiac compression as the mechanism of blood flow. Optimal performance, determined by coronary perfusion pressure, was observed at a sternal force of 100-130 lb (45-59 kg). In the comparative trial, significant differences in the measured CPP were observed between LifeBelt and manual CPR both at 1 min (15+/-8 mmHg versus 10+/-6 mmHg, p<0.05) and 5 min (17+/-4 mmHg versus 13+/-7 mmHg, p<0.02) of chest compression. A greater (p<0.05) ETCO(2), a marker of cardiac output and systemic perfusion, was observed with LifeBelt CPR (20+/-7 mmHg) than with manual CPR (15+/-5 mmHg) at 1 min. Peak Ao pressures were not different between methods. With the device, 86% of animals were resuscitated compared to 76% in the manual group. CONCLUSIONS: Blood flow with the LifeBelt device is primarily the result of cardiac compression. At a sternal force of 100-130 lb (45-59 kg), the device produces greater CPP than well-performed manual CPR during resuscitation from prolonged VF.     

The mechanism of blood flow during closed chest cardiac massage in humans: transesophageal echocardiographic observations

Despite years of research, the mechanism of forward blood flow during closed chest cardiac massage remains controversial. Two theories have been suggested: the cardiac pump theory and the thoracic pump theory. Transesophageal echocardiography offers a new approach for study of the flows and cardiac morphologic features during chest compressions in humans. Case reports are presented to illustrate the use of transesophageal echocardiography during cardiopulmonary resuscitation. The findings included right and left ventricular compression, closure of the mitral valve during compression, opening of the mitral valve during the release phase, and atrioventricular valvular regurgitation during compression, indicating a positive ventricular-to-atrial pressure gradient. These findings suggest that direct cardiac compression was the predominant mechanism of forward blood flow during cardiopulmonary resuscitation in these patients. An understanding of the actual mechanisms involved is necessary if improved cardiopulmonary resuscitative techniques or adjuncts are to be rationally developed for enhancing the outcome of resuscitation.