Do manual chest compressions provide substantial ventilation during prehospital cardiopulmonary resuscitation?

IntroductionChest compressions have been suggested to provide passive ventilation during cardiopulmonary resuscitation. Measurements of this passive ventilatory mechanism have only been performed upon arrival of out-of-hospital cardiac arrest patients in the emergency department. Lung and thoracic characteristics rapidly change following cardiac arrest, possibly limiting the effectiveness of this mechanism after prolonged resuscitation efforts. Goal of this study was to quantify passive inspiratory tidal volumes generated by manual chest compression during prehospital cardiopulmonary resuscitation.Materials and methodsA flowsensor was used during adult out-of-hospital cardiac arrest cases attended by a prehospital medical team. Adult, endotracheally intubated, non-traumatic cardiac arrest patients were eligible for inclusion. Immediately following intubation, the sensor was connected to the endotracheal tube. The passive inspiratory tidal volumes generated by the first thirty manual chest compressions performed following intubation (without simultaneous manual ventilation) were calculated.Results10 patients (5 female) were included, median age was 64 years (IQR 56, 77 years). The median compression frequency was 111 compression per minute (IQR 107, 116 compressions per minute). The median compression depth was 5.6 cm (IQR 5.4 cm, 6.1 cm). The median inspiratory tidal volume generated by manual chest compressions was 20 mL (IQR 13, 28 mL).ConclusionUsing a flowsensor, passive inspiratory tidal volumes generated by manual chest compressions during prehospital cardiopulmonary resuscitation, were quantified. Chest compressions alone appear unable to provide adequate alveolar ventilation during prehospital treatment of cardiac arrest.     

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.     

Comparison of standard CPR versus diffuse and stacked hand position interposed abdominal compression-CPR in a swine model

Interposed abdominal compression cardiopulmonary resuscitation (IAC-CPR) is an innovative basic life support technique requiring no mechanical adjuncts. Optimizing its performance remains a challenge. Hand-position technique over the abdomen during interposed abdominal compression (IAC) may be important. The purpose of this study was to determine if there is a difference in efficacy depending on the type of abdominal hand-position used. Two different hand positions were studied: open hands, placed side by side, resulting in diffuse abdominal compression and stacked hands, with one on top of the other, producing a more focal compression of the abdomen. Thirty swine were cannulated with micromanometer-tipped pressure transducers in the ascending aorta (Ao) and right atrium (RA), and Millar Doppler-tipped catheters in the descending aorta and inferior vena cava (IVC) to determine flow patterns during cardiopulmonary resuscitation (CPR), During CPR there were no differences in aortic systolic or right atrial systolic pressures. Both forms of IAC-CPR produced greater aortic diastolic and right atrial diastolic pressures then standard CPR (STD-CPR) (P<0.05). Coronary perfusion pressures (CPP), however, were not different. Blood flow directions and velocity patterns showed that STD-CPR chest compressions produce caudally directed blood flow in both the descending aorta and the IVC, and that such flows reverse (becoming cranially directed) during the relaxation phase of chest compression. IAC-CPR produced similar blood flow patterns in the aorta and IVC, as seen with STD-CPR. There were no differences in blood flow patterns between the different forms of IAC-CPR. No CPR-produced trauma difference was found. Abdominal hand position (diffuse or stacked) did not affect blood flow in either the aorta or IVC or resuscitation success in this experimental model. There was a trend towards better outcomes with stacked hands IAC-CPR with 90 versus 70% survival with STD-CPR.     

The effects of epinephrine/norepinephrine on end-tidal carbon dioxide concentration, coronary perfusion pressure and pulmonary arterial blood flow during cardiopulmonary resuscitation

End-tidal CO2 concentration correlates with pulmonary blood flow during cardiopulmonary resuscitation and has been claimed to be a useful tool to judge the effectiveness of chest compression. A high concentration of end-tidal CO2 has been related to a better outcome. However, most authors have noticed a decrease in end-tidal CO2 concentration after administration of epinephrine, concomitant with an increase in coronary perfusion pressure and an increased incidence of return of spontaneous circulation. This study was performed to evaluate changes in end-tidal CO2 concentration after injection of vasopressors during cardiopulmonary resuscitation and to investigate the time-course of the response and possible explanations for it. After 1 min of electrically induced cardiac arrest and 5 min of chest compressions, 18 pigs were randomly assigned to receive 0.045 mg kg(-1) epinephrine, 0.045 mg kg(-1) norepinephrine or no drug. After another 4 min of chest compressions the pigs were defibrillated. End-tidal CO2, pulmonary blood flow and coronary perfusion pressure decreased immediately after the induction of cardiac arrest, increased slightly during chest compressions and increased initially to supernormal levels after the return of spontaneous circulation. Injection of epinephrine or norepinephrine during chest compressions decreased end-tidal CO2 51 +/- 2%, (mean +/- S.E.M.), and 43 +/- 1%, respectively, and pulmonary blood flow by 134 +/- 13 and 125 +/- 16%, respectively, within 1 min, simultaneously increasing coronary perfusion pressure from 10 +/- 2 to 45 +/- 5 mm Hg and from 11 +/- 1 to 38 +/- 5 mm Hg, respectively. The coronary perfusion pressure slowly fell, but the effects on end-tidal CO2 and pulmonary blood flow were prolonged. In conclusion, vasopressors increased coronary perfusion pressure and the likelihood of a return of spontaneous circulation, but decreased end-tidal CO2 concentration and induced a critical deterioration in cardiac output and thus oxygen delivery in this model of cardiopulmonary resuscitation.     

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.     

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.     

Changes of aortic dimensions as evidence of cardiac pump mechanism during cardiopulmonary resuscitation in humans.

The mechanism of forward blood flow during cardiopulmonary resuscitation (CPR) remains controversial. We hypothesized that, if the heart acts as a pump, the proximal descending thoracic aorta would be distended during compression by forward blood flow, and would be constricted or remained unchanged if blood flow is generated by increased intrathoracic pressure. Fourteen patients with nontraumatic cardiac arrest underwent transesophageal echocardiography to verify changes in the descending thoracic aorta during standard manual CPR. The aortic dimensions, including cross-sectional area and diameter at the end of compression and relaxation, were measured proximal to, and at the maximal compression site of the descending thoracic aorta. At the maximal compression site, deformation of the descending thoracic aorta was observed during compression in all patients and the ratio of maximal to minimal diameter of the aorta (deformation ratio) decreased during compression compared with relaxation (0.58+/-0.15 vs. 0.81+/-0.11, P=0.001). This suggests eccentric compression of the descending thoracic aorta by external chest compression. The deformation ratio of the descending thoracic aorta proximal to the maximal compression site remained unchanged during compression and relaxation (1.0+/-0.88 vs. 1.0+/-0.9, P=0.345). The cross-sectional area of the descending thoracic aorta proximal to the maximal compression site increased 15% on average during compression compared with relaxation in 12 of 14 patients. In conclusion, deformation of the aorta at the maximal compression site and increase in the cross-sectional area of the proximal aorta suggests that cardiac pumping is the dominant mechanism in generating forward blood flow during CPR in humans.     

Transesophageal echocardiography during cardiopulmonary arrest in the emergency department

Management of patients in cardiopulmonary arrest is challenging and can be resource consuming. Outcomes continue to be poor and physicians may feel a sense of futility when running a resuscitation. Bedside ultrasound has been utilized to guide resuscitations, diagnose correctable cardiac pathology leading to an arrest and has proved to have a prognostic value when utilized in the initial stages of resuscitation. Bedside emergency ultrasound is limited by inability to scan during chest compression and poor image quality in obese patients and those with emphysema. During cardiopulmonary resuscitation pulse checks need to be rapid and leave little time for transducer manipulation during image acquisition. Recent American Heart Association guidelines further stress the need for quality chest compressions and minimizing intervals with no compressions. Transesophageal echocardiography offers high resolution and clarity of images in the vast majority of patients. It allows for constant visualization of the heart, even during chest compressions, cardioversion and other procedures. This case series describes the use of transesophageal echocardiography (TEE) during cardiac arrest by emergency physicians. The cases illustrate some of the potential benefits of TEE during cardiopulmonary arrest.     

Mechanical devices for cardiopulmonary resuscitation

PURPOSE OF THE REVIEW: For over 40 years, manual chest compressions have been the foundation of cardiopulmonary resuscitation and recent studies have clearly reconfirmed the hemodynamic significance of delivering consistent, high-quality, infrequently-interrupted chest compressions. However, there remain multiple inadequacies in the actual delivery of manual chest compressions during cardiopulmonary resuscitation. One potential solution is use of adjunct mechanical devices. RECENT FINDINGS: Two different methods of accessory chest compression techniques recently have demonstrated enhanced short-term survival. The active compression-decompression device is a hand-held, manually operated suction device applied to the center of the chest wall. In tandem with an impedance threshold (airway) device, active compression-decompression has shown a 65% improvement in 24-hour survival rates (compared with standard cardiopulmonary resuscitation) in a randomized out-of-hospital clinical trial (n = 210). The second device, called Auto-Pulse CPR is an automated machine that uses a load-distributing, broad compression band that is applied across the entire anterior chest. A recent out-of-hospital retrospective case-control study (n = 162) also revealed improved short-term survival. SUMMARY: High quality chest compressions during cardiopulmonary resuscitation are critical elements in effecting successful resuscitation following a cardiac arrest. Recent studies utilizing adjunct mechanical devices have not only revealed significant increases in the effectiveness of chest compressions, including improved hemodynamics in both animal models and human studies, but also improvements in short-term human survival in the clinical setting. It is hoped that these promising findings will eventually be corroborated in terms of improved neurologically intact, long-term patient survival. Clinical trials are currently underway to validate such efficacy.     

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.     

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.     

Cerebral cortical microvascular flow during and following cardiopulmonary resuscitation after short duration of cardiac arrest

AIM: To examine changes in cerebral cortical macro- and microcirculation and their relationship to the severity of brain ischaemia during and following resuscitation from a short duration of cardiac arrest. METHODS: Bilateral cranial windows were created in eight domestic pigs weighing 41+/-1 kg, exposing the frontoparietal cortex for orthogonal polarization spectral imaging together with estimation of cortical-tissue partial pressure of carbon dioxide, a quantitator of the severity of cerebral ischaemia. After 3 min of untreated ventricular fibrillation, cardiopulmonary resuscitation was begun and continued for 4 min before defibrillation. Aortic pressure, end-tidal and cortical-tissue partial pressure of carbon dioxide, and cortical microcirculatory blood flow in vessels of less and more than 20 microm in diameter were continuously measured. RESULTS: Cerebral microcirculatory blood flow progressively decreased over the 3-min interval that followed onset of ventricular fibrillation. Chest compression restored cortical microvascular flow to approximately 40% of the pre-arrest value. Following return of spontaneous circulation, microvascular flow velocity was restored to baseline values over 3 min. Reversal of cerebral ischaemia with normalisation of cerebral cortical-tissue partial pressure of carbon dioxide occurred over 7 min after resuscitation. Cortical microcirculatory blood flow in microvessels less than 20 microm was highly correlated with flow in vessels more than 20 microm together with mean aortic pressure and end-tidal partial pressure of carbon dioxide. CONCLUSION: Cerebral cortical microcirculatory flow ceased only 3 min after onset of cardiac arrest. Flow was promptly restored to 40% of its pre-arrest value after start of chest compression. After resuscitation, both macro- and microcirculatory flows were fully restored over 3 min, but cerebral ischaemia reversed more slowly.     

Calcium-entry blockers during porcine cardiopulmonary resuscitation

1. Calcium-entry blockers increase the intramyocardial pH and decrease the intramyocardial Pco2 of ischaemic canine myocardium. However, the evidence documenting improvements in myocardial acidosis and in myocardial resuscitability after administration of calcium-entry blockers during cardiac arrest is incomplete. We therefore compared the effects of verapamil (0.05 mg/kg) and diltiazem (0.075 mg/kg) with those of saline placebo in an established porcine model of cardiac arrest and cardiopulmonary resuscitation. 2. After verapamil, six of 11 animals were successfully resuscitated; after diltiazem, five of 10; and after saline placebo, six of 10. Coronary perfusion and mean aortic pressures together with end-tidal CO2 concentration during precordial compression were predictive of resuscitation, independently of the drug or placebo. 3. Coronary vein pH decreased to 6.91 +/- 0.06 units (mean +/- SEM) with concurrent increases in PCO2 to levels exceeding 100 mmHg. Coronary vein lactate increased to a maximum of 7.5 +/- 0.6 mmol/l. Coronary vein acidaemia was accompanied by decreases in intramyocardial pH to 6.64 +/- 0.06 units. However, each of these differences between success and failure of resuscitation was unrelated to treatment with calcium-entry blockers. 4. Accordingly, neither verapamil nor diltiazem selectively altered coronary perfusion pressure, attenuated intramyocardial acidosis or improved resuscitability after porcine cardiac arrest and cardiopulmonary resuscitation.     

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.     

Quantification of ventilation volumes produced by compressions during emergency department cardiopulmonary resuscitation

Background

Clinical investigations have shown improved outcomes with primary compression cardiopulmonary resuscitation strategies. It is unclear whether this is a result of passive ventilation via chest compressions, a low requirement for any ventilation during the early aspect of resuscitation or avoidance of inadvertent over-ventilation.

Left Ventricular Compressions Improve Hemodynamics in a Swine Model of Out-of-Hospital Cardiac Arrest

Introduction: We hypothesized that chest compressions located directly over the left ventricle (LV) would improve hemodynamics, including coronary perfusion pressure (CPP), and return of spontaneous circulation (ROSC) in a swine model of cardiac arrest. Methods: Transthoracic echocardiography (echo) was used to mark the location of the aortic root and the center of the left ventricle on animals (n = 26) which were randomized to receive chest compressions in one of the two locations. After a period of ten minutes of ventricular fibrillation, basic life support (BLS) with mechanical cardiopulmonary resuscitation (CPR) was initiated and performed for ten minutes followed by advanced cardiac life support (ACLS) for an additional ten minutes. During BLS the area of maximal compression was verified using transesophageal echo. CPP and other hemodynamic variables were averaged every two minutes. Results: Mean CPP was not significantly higher in the LV group during all time intervals of resuscitation; mean CPP was significantly higher in the LV group during the 12–14 minute interval of BLS and during minutes 22–30 of ACLS (p < 0.05). Aortic systolic and diastolic pressures, right atrial systolic pressures, and end-tidal CO2 (ETCO2) were higher in the LV group during all time intervals of resuscitation (p < 0.05). Nine of the left ventricle group (69%) achieved ROSC and survived to 60 minutes compared to zero of the aortic root group (p < 0.001). Conclusions: In our swine model of cardiac arrest, chest compressions over the left ventricle improved hemodynamics and resulted in a greater proportion of animals with ROSC and survival to 60 minutes.     

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.     

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.     

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.     

Cardiac, thoracic, and abdominal pump mechanisms in cardiopulmonary resuscitation: studies in an electrical model of the circulation

To investigate alternative mechanisms generating artificial circulation during cardiopulmonary resuscitation (CPR), an electrical model of the circulation was developed. 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. Three modes of creating artificial circulation were studied: cardiac pump (CP), in which the atria and ventricles of the model were pressurized simultaneously; thoracic pump (TP), in which all intrathoracic elements of the model were pressurized simultaneously; and abdominal pump (AP), in which the abdominal aorta and inferior vena cava of the model were pressurized simultaneously. Flow was greatest with the CP, less with the TP, and least with the AP mechanism. However, the AP could be practically combined with either the CP or TP by interposition of abdominal compressions between chest compressions (IAC-CPR). Our model predicts that this combined method can substantially improve artificial circulation, especially when cardiac compression does not occur and chest compression invokes only the thoracic pump mechanism.