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During cardiopulmonary resuscitation (CPR), the electrocardiogram (ECG) is often obscured by noise. This noise is in the form of baseline variations in the ECG, which often necessitate stopping chest compressions to adequately assess the ECG. Because survival from cardiac arrest has been shown to be related to blood flow generated during CPR, and because interruption of chest compressions will reduce blood flow, survival may be compromised by these interruptions. Three possible sources for the noise were considered: the heart, which is deformed during CPR, which may introduce a mechanical-electrical interaction and alter the normal electrical pattern of the heart; the thoracic cavity, which may have large impedance variations because of CPR and thereby modulate the ECG; and the skin-electrode interface, which may be mechanically disturbed during CPR and thus produce polarization potentials that cause additional noise. CPR studies were performed on five dogs by using four different test conditions and six different types of electrodes. The test conditions were: electrode motion, which allowed mechanical disturbances of the skin-electrode interface without altering the thoracic impedance or deforming the heart; vest CPR; manual CPR; and respiration. The myocardial ECG, the bipolar and unipolar surface ECGs, and the thoracic impedance were monitored. Different types of surface ECG electrodes were used to determine whether the noise was dependent on electrode type or size. There were no baseline variations in the myocardial ECG during any of the test conditions. The thoracic impedance did vary during CPR, but the variations were temporally uncorrelated to the baseline variations in the ECG, and the variations were of similar magnitude as the variations caused by respiration, which produced no baseline changes in the ECG. Finally, the magnitude of the baseline variations in the ECG was substantially different for electrodes of different sizes and shapes, and electrode motion produced baseline variations that were identical to those produced during CPR. Therefore, it was concluded that the source of the noise in the ECG during CPR is the skin-electrode interface and, specifically, that the noise is related to the electrical properties of the electrode.

Both laboratory and clinical investigators contribute to the multidisciplinary knowledge base of resuscitation science. While diversity can be a strength, it can also be a hindrance because of the lack of a common language and poor communication among investigators. Modern cardiopulmonary resuscitation (CPR) research depends on the use of animal models that are designed to simulate cardiac arrest in humans.1 2 Such models are used to explore important new treatments and to refine protocols used in standard interventions, including doses of drugs, chest compression techniques, defibrillation energies, and cerebral resuscitation, before they are applied to humans.3 When favorable results are reported in animal models, the new or refined techniques are often implemented soon afterward in human victims of cardiac arrest. Unfortunately, the results obtained in one laboratory may not be reproducible in another laboratory or in human trials. For example, high-dose epinephrine therapy significantly improves survival in most animal models of cardiac arrest but does not improve survival in humans.4 5 6 7 In addition, some animal studies have documented the efficacy of administering bicarbonate during cardiac arrest, while others have shown it to be ineffective or deleterious.8 Some of these differences are to be expected because an animal simulation is not a perfect model of cardiac arrest in humans. However, it is likely that some of these conflicting results are due to differences in experimental methods and laboratory model design. Variations in study design, such as the quality of chest compressions and ventilation, definitions of variables, or time intervals between an event and the beginning of therapy, are probably responsible for many of the inconsistencies and contradictions reported. The lack of standardization and the use of nonuniform terminology in reports of studies of cardiac arrest in humans have been described as a “Tower of Babel.” …

[Halperin HR, Chandra NC, Levin HR, Rayburn BK, Tsitlik JE: Newer methods of improving blood flow during CPR. Ann Emerg Med May 1996;27:553-562.]

More than 300,000 people die each year of cardiac arrest. Studies have shown that raising vascular pressures during cardiopulmonary resuscitation (CPR) can improve survival and that vascular pressures can be raised by increasing intrathoracic pressure.To produce periodic increases in intrathoracic pressure, we developed a pneumatically cycled circumferential thoracic vest system and compared the results of the use of this system in CPR (vest CPR) with those of manual CPR. In phase 1 of the study, aortic and right-atrial pressures were measured during both vest CPR (60 inflations per minute) and manual CPR in 15 patients in whom a mean (+/- SD) of 42 +/- 16 minutes of initial manual CPR had been unsuccessful. Vest CPR was also carried out on 14 other patients in whom pressure measurements were not made. In phase 2 of the study, short-term survival was assessed in 34 additional patients randomly assigned to undergo vest CPR (17 patients) or continued manual CPR (17 patients) after initial manual CPR (duration, 11 +/- 4 minutes) had been unsuccessful.In phase 1 of the study, vest CPR increased the peak aortic pressure from 78 +/- 26 mm Hg to 138 +/- 28 mm Hg (P0.001) and the coronary perfusion pressure from 15 +/- 8 mm Hg to 23 +/- 11 mm Hg (P0.003). Despite prolonged unsuccessful manual CPR, spontaneous circulation returned with vest CPR in 4 of the 29 patients. In phase 2 of the study, spontaneous circulation returned in 8 of the 17 patients who underwent vest CPR as compared with only 3 of the 17 patients who received continued manual CPR (P = 0.14). More patients in the vest-CPR group than in the manual-CPR group were alive 6 hours after attempted resuscitation (6 of 17 vs. 1 of 17) and 24 hours after attempted resuscitation (3 of 17 vs. 1 of 17), but none survived to leave the hospital.In this preliminary study, vest CPR, despite its late application, successfully increased aortic pressure and coronary perfusion pressure, and there was an insignificant trend toward a greater likelihood of the return of spontaneous circulation with vest CPR than with continued manual CPR. The effect of vest CPR on survival, however, is currently unknown and will require further study.

Cardiac arrest causes a rapid loss of cerebral adenosine triphosphate [corrected] (ATP) and a decrease in cerebral intracellular pH (pHi). Depending on the efficacy of cardiopulmonary resuscitation (CPR), cerebral blood flow levels (CBF) ranging from near zero to near normal have been reported experimentally. Using 31P magnetic resonance spectroscopy, the authors tested whether experimental CPR with normal levels of cerebral blood flow can rapidly restore cerebral ATP and pHi despite the progressive systemic acidemia associated with CPR. After 6 min of ventricular fibrillation in six dogs anesthetized with fentanyl and pentobarbital, ATP was reduced to undetectable concentrations and pHi decreased from 7.11 +/- 0.02 to 6.28 +/- 0.09 (+/- SE) as measured by 31P magnetic resonance spectroscopy. Application of cyclic chest compression by an inflatable vest placed around the thorax and infusion of epinephrine (40 micrograms/kg bolus plus 8 micrograms/kg/min, intravenously) maintained cerebral perfusion pressure greater than 70 mmHg for 50 min with the dog remaining in the magnet. Prearrest cerebral blood flows were generated. Cerebral pHi recovered to 7.03 +/- 0.03 by 35 min of CPR, whereas arterial pH decreased from 7.41 +/- 0.4 to 7.08 +/- 0.04 and cerebral venous pH decreased from 7.29 +/- 0.03 to 7.01 +/- 0.04. Cerebral ATP levels recovered to 86 +/- 7% (+/- SE) of prearrest concentration by 6 min of CPR. There was no further recovery of ATP, which remained significantly less than control. Therefore, in contrast to hyperemic reperfusion with spontaneous circulation and full ATP recovery, experimental CPR may not be able to restore ATP completely after 6 min of global ischemia despite restoration of CBF and brain pHi to prearrest levels.

Animal studies have demonstrated that ventilation can be deferred for several minutes in witnessed arrest if chest compression is initiated promptly. It is unknown if this observation is also valid in situations of a “prolonged down time”. To assess whether immediate ventilation was essential following a prolonged down time arrest, six 20-30 kg, dogs were studied following ventricular fibrillation (VF). Chest compression (no ventilation) at 80-90/min was initiated after 6 min. Aortic pressure (pr) and blood gases were monitored. Pre-VF aortic pr; pH: PCPCO2 and O2 saturation (%02 sat) at room air were 136 ± 9.8/109 ± 8 mmHg; 7.38 ± 0.03; 37.9 ± 2.3; 97.5 ± 0.5% (M ± SEM). Following a 6 min downtime (DTl. there was no substantial change in arterial blood gases (graphs below). After 2 min of chest compression only the corresponding values were still 55 ± 13/21 ± 7 mmHg, 7.3 ± 0.0, 44.6 ± 1.6 and 90.8 ± 3.8%. Download : Download high-res image (65KB) Download : Download full-size image These data suggest that in a dog model. even following a prolonged down time, chest compression alone can maintain adequate gas exchange to sustain 02 saturation g90% for g2 minutes. The need for immediate ventilation during resuscitation must be reexamined.

BACKGROUND Fear of infection limits the willingness of laymen to do cardiopulmonary resuscitation (CPR). This study assessed the time course of change in arterial blood gases during resuscitation with only chest compression (no ventilation) in an effort to identify the time for which ventilation could be deferred. METHODS AND RESULTS Aortic pressures and arterial blood gases were monitored in seven 20- to 30-kg dogs in ventricular fibrillation (VF) at 2-minute intervals during chest compression alone (no ventilation) at 80 to 100 compressions per minute. Before the induction of ventricular fibrillation, all animals were intubated and ventilated with room air, 10 mL/kg. The endotracheal tube was removed when VF was induced. Pre-VF arterial pH, PCO2, and O2 saturation were (mean +/- SEM) 7.39 +/- 0.02, 27.0 +/- 1.5 mm Hg, and 97.5 +/- 0.5%, respectively, with aortic pressures being 143.2 +/- 5.7/116.2 +/- 4.6 mm Hg. At 4 minutes of chest compression alone, the corresponding values were 7.39 +/- 0.03, 24.3 +/- 3.1 mm Hg, and 93.9 +/- 3.0%, with an arterial pressure of 48.1 +/- 7.7/22.6 +/- 3.9 mm Hg. Mean minute ventilation during the fourth minute of CPR, measured with a face mask-pneumotachometer, was 5.2 +/- 1.1 L/min. CONCLUSIONS These data suggest that in the dog model of witnessed arrest, chest compression alone during CPR can maintain adequate gas exchange to sustain O2 saturation > 90% for > 4 minutes. The need for immediate ventilation during witnessed arrest should be reexamined.

Pressures were measured in the right atrium, thoracic aorta, and pleural space during conventional cardiopulmonary resuscitation (CPR) and simultaneous ventilation compression cardiopulmonary resuscitation (SVC-CPR) in dogs, pigs, and a baboon. During both forms of closed chest resuscitation, the changes in atrial and aortic pressures were virtually identical over a range of 0-90 mm Hg and essentially equaled the change in pleural pressure measured at the most lateral portion of the chest cavity. During internal cardiac massage, there was no consistent relationship between right atrial and aortic pressures. However, even after the chest had been opened, the hemodynamics of external chest compression could be restored by the creation of a closed, air filled cavity surrounding the heart and great vessels. Thus, elevation of intrathoracic pressure, not direct cardiac compression, is essential to and determine circulation of blood during CPR.

Prior studies in dogs indicate that (1) blood flow during cardiopulmonary resuscitation results from the induced rise in intrathoracic pressure rather than from direct cardiac compression, and (2) maneuvers that increase intrathoracic pressure lead to increased carotid blood flow. Therefore, a system was devised for administering cyclical increases in intrathoracic pressure without lung overinflation for use during cardiac arrest. Ventilation at high airway pressure (60 to 100 mm Hg) was performed simultaneously with chest compression at a rate of 40/min in seven dogs with cardiac arrest. Airway pressure returned to the atmospheric level between compression-ventilation periods to allow venous return. This new technique was compared with conventional cardiopulmonary resuscitation both with and without sustained abdominal compression by binding. Peak chest compression force was held constant during all forms of resuscitation. Carotid blood flow was higher during simultaneous compression-ventilation resuscitation than with conventional resuscitation both without abdominal binding (mean ± standard error of the mean 18.7 ± 4.7 versus 5.1 ± 1.08 ml/min, p

The goals of this study were to quantify the effects of epinephrine on myocardial and cerebral blood flow during conventional cardiopulmonary resuscitation (CPR) and CPR with simultaneous chest compression-ventilation and to test the hypothesis that epinephrine would improve myocardial and cerebral blood flow by preventing collapse of intrathoracic arteries and by vasoconstricting other vascular beds, thereby increasing perfusion pressures. Cerebral and myocardial blood flow were measured by the radiolabeled microsphere technique, which we have previously validated during CPR. We studied the effect of epinephrine on established arterial collapse during CPR with simultaneous chest compression-ventilation with the abdomen bound or unbound. Epinephrine reversed arterial collapse, thereby eliminating the systolic gradient between aortic and carotid pressures and increasing cerebral perfusion pressure and cerebral blood flow while decreasing blood flow to other cephalic tissues. Epinephrine produced higher cerebral and myocardial perfusion pressures during CPR with simultaneous chest compression-ventilation when the abdomen was unbound rather than bound because abdominal binding increased intracranial and venous pressures. In other experiments we compared the effect of epinephrine on blood flow during 1 hr of either conventional CPR or with simultaneous chest compression-ventilation with the abdomen unbound. Epinephrine infusion during conventional CPR produced an average cerebral blood flow of 15 ml/min . 100 g (41 +/- 15% of control) and an average myocardial blood flow of 18 ml/min . 100 g (15 +/- 8% of control). In our previous studies, cerebral and myocardial blood flow were less than 3 +/- 1% of control during conventional CPR without epinephrine. Although flows during CPR with simultaneous chest compression-ventilation without epinephrine were initially higher than those during conventional CPR, arterial collapse developed after 20 min, limiting cerebral and myocardial blood flow. The use of epinephrine throughout 50 min of CPR with simultaneous chest compression-ventilation maintained cerebral blood flow at 22 +/- 2 ml/min . 100 g (73 +/- 25% control) and left ventricular blood flow at 38 +/- 9 ml/min . 100 g (28 +/- 8% control). The improved blood flows with epinephrine correlated with improved electroencephalographic activity and restoration of spontaneous circulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. We developed a mathematical model that predicts that 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, however, the model predicts that flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. The model was validated for direct cardiac compression by studying the hemodynamics of cyclic cardiac deformation following thoracotomy in four anesthetized, 21-32-kg dogs. As predicted by the model, there was no change in myocardial or cerebral perfusion pressures when the duration of compression was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. The model was validated for intrathoracic pressure changes by studying the hemodynamics produced by a thoracic vest (vest CPR) in eight dogs. The vest contained a bladder that was inflated and deflated. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. As predicted by the model and opposite to direct cardiac compression, there was no change in perfusion pressures when the rate was increased from 60 to 150/min at a constant duration of 45% of the cycle. Manual CPR was then studied in eight dogs. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres and behaved as predicted from the model of intrathoracic pressure, not direct cardiac compression. At nearly constant peak sternal force (378-426 N), flow was significantly increased when the duration of compression was increased from short (13%-19% of the cycle) to long (40%-47%), at a rate of 60/min. Flow was unchanged, however, for an increase in rate from 60 to 150/min at constant compression duration. In addition, myocardial and cerebral flow correlated with their respective perfusion pressures.(ABSTRACT TRUNCATED AT 400 WORDS)

Elevation of intrathoracic pressure during cardiopulmonary resuscitation generates carotid pressure and flow, but also increases intracranial pressure. This increase in intracranial pressure may limit cerebral blood flow. Therefore, we performed studies designed to quantify the extent of this transmission and to identify the mechanism of transmission of intrathoracic pressure to the intracranial space during cardiopulmonary resuscitation in dogs. Intracranial pressure increased during the chest compression phase of all modes of cardiopulmonary resuscitation tested. During simultaneous compression-ventilation cardiopulmonary resuscitation, change in intracranial pressure (mm Hg) = 0.33 change in intrathoracic pressure (mm Hg) + 2.02 (r = 0.86) and was not significantly different from the relationship observed during conventional cardiopulmonary resuscitation. The magnitude of transmission of intrathoracic pressure to the intracranial space was increased by binding the abdomen and by raising the baseline intracranial pressure. No single route accounted for transmission of intrathoracic pressure to the intracranial space during cardiopulmonary resuscitation. Intracranial pressure fluctuations were unrelated to either carotid arterial or jugular venous pressure, and were found instead to be the result of pressure transmission by blood in non-valved veins and by cerebrospinal fluid. This was determined by three maneuvers. First, obstruction of cerebrospinal fluid flow by ligation of the cervical spinal cord reduced intracranial pressure (P less than 0.001) and made the change in intracranial pressure equivalent to pressure changes at the confluence of the intracranial venous sinuses, without affecting pressure changes at the confluence of the intracranial venous sinuses. Second, ligation of the cervical spinal cord and one of the two longitudinal vertebral veins adjacent to the cervical cord reduced the pressure changes in the intracranial space and at the confluence of the intracranial venous sinuses to about 60% of the levels observed when the cervical cord alone was ligated. Thus, the non-valved longitudinal vertebral veins appear to be the vascular channels of critical importance to pressure transmission. Finally, pressure changes in the thoracic cerebrospinal fluid were increased (P less than 0.05) by cord ligation, even after exsanguination minimized pressure transmission via blood-filled channels, indicating direct transmission of intrathoracic pressure through intervertebral foramina to the cerebrospinal fluid.(ABSTRACT TRUNCATED AT 400 WORDS)

Simultaneous compression-ventilation Cardiopulmonary resuscitation has been shown to produce high peripheral arterial pressure and flows in comparison with conventional Cardiopulmonary resuscitation. To evaluate further the mechanisms responsible for blood flow during the large cyclical changes in intrathoracic pressure with simultaneous compression-ventilation Cardiopulmonary resuscitation this study assessed (1) the timing of blood flow from the lungs toward the aorta and periphery, and (2) the timing and mechanisms of return of blood from the periphery to the heart and lungs. After induction of ventricular fibrillation in dogs, radionuclide angiography was performed and pulmonary flow velocity measured during simultaneous compression-ventilation Cardiopulmonary resuscitation with each high (70 to 100 mm Hg) intrathoracic pressure phase lasting from 0.9 to 3.6 seconds. The abdomen was bound. Carotid flow during resuscitation was 27 ± 5 percent (mean ± standard error of the mean) of the value before cardiac arrest. With injection of technetium-99m albumin into the right atrium, the radionuclide activity cleared the right atrium only during periods of tow intrathoracic pressure between the high intrathoracic pressure periods. There was a simultaneous increase in lung activity during the periods of low pressure. Thus, blood left the right atrium and entered the lungs during these low pressure periods. Flow velocity recordings in the pulmonary artery confirmed that pulmonary flow occurred mainly during low intrathoracic pressure. There was negligible retrograde pulmonary flow during high intrathoracic pressure. This feature, together with a lack of increase in right atrial counts, suggests that the pulmonary valve was probably closed during high intrathoracic pressure. After injection of technetium-99m albumin into the distal pulmonary bed through a wedged catheter, 29.7 ± 8 percent (probability [p] Thus, with simultaneous compression-ventilation Cardiopulmonary resuscitation, blood flow into the lungs occurs during periods of low intrathoracic pressure and from the lungs into the left ventricle and aorta during periods of high intrathoracic pressure. The heart functions merely as a passive conduit for blood flow to and from the lungs.

The determination that blood can move during cardiopulmonary resuscitation because of imposed changes in intrathoracic pressure has led to the construction and testing of mechanical devices for increasing intrathoracic pressure fluctuations over those obtained by manual means. These mechanical systems have required high-pressure ventilation simultaneous with compression of the chest to augment blood flow. Their usefulness has been limited, however, because of the requirement for endotracheal intubation and complex devices. Similar systems have also been used to generate intrathoracic pressure changes timed to the cardiac cycle to aid the failing, but beating, heart. A system was developed that can produce high intrathoracic pressure without simultaneous ventilation by using a vest that is placed around the thorax. The vest contains a bladder that is rapidly inflated and deflated by the programmable pneumatic generator. Air flows into and out of the bladder by the proper sequencing of large-bore three-way and two-way solenoid valves that are connected in series. A microcomputer-based controller is used to sequence the valves. The programmable pneumatic generator inflates the bladder more rapidly and to higher pressures than previous systems. The programmable pneumatic generator has been used in studies of cardiopulmonary resuscitation (heart arrested) and circulatory assistance (heart beating, but function depressed).

A system has been developed that generates cyclic fluctuations in intrathoracic pressure for use in cardiopulmonary resuscitation (CPR). The system was realized with a pneumatic vest, which is placed around the thorax, and an inflation system. The vest contains a bladder that is cyclically inflated and deflated. Air flows into and out of the bladder by the proper sequencing of solenoid valves. A safety system monitors the pressure in the bladder and can vent pressure from the bladder and disable operation of the valves if a malfunction occurs. This systems uses real-time control of vest pressure to overcome the vast-pressure variations of older systems, and is safer than previous systems. >

Sternal displacement during CPR was measured in 11 adults and 2 manikins (Recording Resusci Anne) while the chest was compressed with variable maximum pulse compression force at a rate of 60/min with compression duration of 0.5-0.6 sec. In 10 patients, the pulsatile sternal elastic characteristic can be satisfactorily described with a 2nd degree polynomial F = beta Ds + gamma D2s, where beta = 54.9 +/- 29.4 (mean +/- SD) N/cm is the pulsatile initial elasticity and gamma = 10.8 +/- 4.1 N/cm2 is the posterior resiliency. The sternal characteristics of manikins were linear F = kDs with high elasticity constants, k = 131 and 142 N/cm. Therefore, the manikins tested differ significantly in elasticity characteristics from the human chest during resuscitation. In general, the manikin: (1) has markedly greater stiffness at the onset of compression, and (2) maintains a linear stiffness throughout the usual range of displacement, rather than becoming stiffer with greater chest displacement.

Recent studies have demonstrated that for the same chest compression force during mechanical cardiopulmonary resuscitation (CPR), the carotid artery-to-jugular vein pressure gradient and carotid blood flow are increased when the phasic rise of intrathoracic pressure is enhanced by abdominal binding and simultaneous ventilation at high airway pressure with each chest compression (SCV). The objective of the present study was to assess whether cerebral blood flow is also enhanced, since it is known that fluctuations in intrathoracic pressure are transmitted to the intracranial space and affect intracranial pressure (ICP). In two series of pentobarbital-anesthetized dogs, one of two CPR techniques was initiated immediately after inducing ventricular fibrillation. Brain blood flow was measured by the radiolabeled microsphere technique immediately before cardiac arrest and at 1 and 3 minutes after commencing CPR. Evidence of adequate mixing of spheres and lack of sedimentation under these low-flow conditions was verified by correlation with brain venous outflow, comparison of the arterial concentration-time profile of spheres and a nonsedimentary marker (thallium-201 in solution), and use of multiple arterial sampling sites. During SCV CPR with abdominal binding, mean carotid artery pressure (60 +/- 3 mm Hg) was higher than that during conventional CPR (25 +/- 2 mm HG). Pulsations of ICP occurred that were in phase with chest compression and greater than jugular venous pressure. Mean ICP was higher during SCV (46 +/- 2 mm Hg) than conventional CPR (20 +/- 2 mm Hg). However, the net brain perfusion pressure gradient (carotid artery pressure - ICP) was greater with SCV (14 +/- 3 mm Hg) than with conventional CPR (5 +/- 0.4 mm Hg). Cerebral blood flow was significantly greater during SCV CPR (32 +/- 7% of prearrest cerebral flow) than during conventional CPR (3 +/- 2%). We conclude that SCV CPR combined with abdominal binding substantially improved brain perfusion by enhancing cerebral perfusion pressure in this experimental model.