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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.]

Reports of clinical improvement in human studies of dynamic cardiomyoplasty lack support by consistent objective hemodynamic evidence. Animal studies have also yielded conflicting results, likely due to nonuniform models, particularly the use of unconditioned wraps, and to limitations in commonly used study modalities caused by exaggerated heart motion during wrap stimulation. Our purpose was to assess the primary functional properties of the heart wrapped by conditioned muscle using pressure-volume relation analysis based on conductance catheter volume data. Compared with the unstimulated state, 1:1 stimulation caused an increase in contractility and decreases in end-diastolic volume and stroke work. Assisted beats during 1:2 stimulation showed an increase in contractility and a decrease in end-diastolic volume. Unassisted beats (1:2) showed decreases in end-diastolic volume and stroke work. There was no augmentation of cardiac output or ejection fraction with stimulation (1:1 or 1:2). We conclude that in the nonfailing heart, increased contractility does not augment cardiac output, ejection fraction, and stroke work because of a simultaneous decrease in end-diastolic volume. These changes in contractility and end-diastolic volume may prove therapeutic for dilated cardiomyopathy.

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.

A device for monitoring a patient or pacing a patient is disclosed which can safely operate in a MRI system. The device uses unique RF filtering and shielding to attenuate voltages on the leads resulting from the high frequency RF signals produced in the MRI. The device is uniquely shielded to prevent induced currents from disrupting the amplifying and processing electronics. The device uses an optional secondary low pass or band reject filter to eliminate interference from the MRI's gradient magnetic field. The device uses optional inductors placed close to electrodes to limit RF currents through the electrodes. Several embodiments of the RF filter are taught which depend on the number of sensing leads, whether the leads are shielded, whether the RF filter is contained in the electronic shielded housing or whether single or multistage filtering is employed. The device may operate as an extended ECG monitor or may be an implantable MRI safe pacemaker.

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