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In an effort to improve the efficiency of cardiopulmonary resuscitation (CPR), a new inspiratory impedance threshold valve has been developed to enhance the return of blood to the thorax during the chest decompression phase. This new device enhances negative intrathoracic pressure during chest wall recoil or the decompression phase, leading to improved vital organ perfusion during both standard CPR and active compression-decompression CPR. With active compression-decompression CPR, addition of the impedance threshold valve results in sustained diastolic pressures of >55 mm Hg in patients in cardiac arrest. The new valve shows promise for patients in asystole or shock refractory ventricular fibrillation, when enhanced return of blood flow to the chest is needed to "prime the pump." The potential long-term benefits of this new valve remain under study.

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SUMMARY To corroborate thiopental protection from cerebral anoxia after cardiopulmonary arrest, 23 sedated, curarized, adult dogs were asphyxiated by plugging the endotracheal tube. Cardiopulmonary resuscitation (CPR) was started 7 minutes after electrocortical silence. Twelve animals received no other treatment (controls), 10 regained consciousness and spontaneous respirations, but remained decerebrate, blind, unable to drink or feed. Two dogs returned to a normal neurologic state. Ten dogs were treated with thiopental after CPR, 7 received 15 mg/kg the first minute, followed by 23 mg/kg over 1 hour; 3 received 60 mg/kg in the first 3 minutes, followed by 30 mg/kg over 1 hour. Except for 1 dog in the low-dose group that recovered neurologically, thiopental-treated dogs showed no neurological or survival improvement over the controls.Stroke, Vo! 10, No 2, 1979LABORATORY DEMONSTRATION of central nervous system recovery after prolonged ischemic anoxic injury 1 has resulted in renewed interest in the treatment of post-anoxic states.Several studies have demonstrated the effectiveness of barbiturate anesthetics in ameliorating the effects of focal ischemic injury.2 Clinically, patients may do surprisingly well after deep barbiturate coma and anoxia.3 Several laboratories have reported beneficial effects of barbiturates in models of global anoxic injury. 49 We attempted to demonstrate a similar benefit in a model closely paralleling the clinical situation of hypoxic cardiac arrest. MethodsTwenty-two, 8 to 16 kg adult mongrel dogs were fasted for 12 hours prior to the experiment. They were anesthetized with a combination of fentanyl and droperidol (Innovar-Vet), 0.1 cc/kg body weight and paralyzed with pancuronium bromide, 0.1 mg/kg. They were then intubated and placed on a piston ventilator with an in-line CO 2 meter (Godart Capnograph). Tidal volume and respiratory rate were adjusted to achieve an expired CO 2 content of 3.5 to 4.5% throughout the experiment. Biparietal scalp EEG leads, ECG electrodes, and a rectal temperature probe were attached. Intravenous dextrose 5% in water, 60 cc per hour, was given throughout the experiment (approximately 5 hours). Normal saline with 1000 U heparin/1 was used as a flushing solution. Through an inguinal incision, a Swan-Ganz catheter was passed via the femoral vein and placed in the right atrium as confirmed by pressure tracings. A femoral arterial line was inserted into the aorta and attached to a Statham strain gauge. Arterial blood pressure (AP), heart rate, and EEG were monitored throughout the experiment.The animals were allowed to emerge from anesthesia to the point of regaining a pedal withdrawal reflex and minimal respiratory efforts. At this time, pancuronium was re-administered and the endotracheal tube plugged after emptying the chest by compression. The EEG was observed until it became isoelectric. This state was maintained for 7 minutes. At that time, standard cardiopulmonary resuscitation was begun with Ambu bag ventilation with 100% oxygen and closed chest card...