James A. Schena
Harvard University
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Featured researches published by James A. Schena.
Critical Care Medicine | 1984
James A. Schena; John E. Thompson; Robert K. Crone
We found that altering aspirating flow rate (ASR) and sample tubing length (STL) affected the response time and capnogram of 2 different side-stream capnometers. Increased flow rate shortened rise time, transit time, and total delay time (TDT), whereas increased STL increased transit and TDTs but not rise time. Increasing rise time pushed the ascending limb of the capnogram to the right. Peak and baseline PCO2 values were accurate only when TDT did not exceed respiratory cycle time (RCT). Awareness of the potential for artifactual changes in the capnogram will avoid their misinterpretation as physiologic events.
Anesthesiology | 1987
Marc B. Hershenson; P. Pearl O'Rourke; James A. Schena; Robert K. Crone
A critical level of oxygen transport has been defined as the level which is required to maintain tissue oxygen uptake (VO2. If halothane reduces the susceptibility to hypoxia, it should lower the critical levels of both O2 delivery (DO2 and arterial oxygen tension (po2). To test this hypothesis, 12 newborn lambs were anesthetized with either fentanyl and pancuronium (control group) or fentanyl, pancuronium, and 1.1% (1 MAC) halothane (halothane group). Baseline measurements of hemoglobin, cardiac output (CO), arterial and mixed-venous Po2, and saturation were obtained on FIo2 1.0, and repeated with FIo2, 21, .15, and .10. O2 delivery (CO X CaO2) and O2 consumption were calculated from measured parameters. Critical levels were selected using a system of repetitive linear regression. Halothane decreased baseline O2 consumption (12.1 ± 0.7 to 8.4 ± 0.4 cc.kg−1. min−1, x ± SEM, P < .001, unpaired t test), but caused similar reductions in cardiac output (235 ± 15 to 132 ± 15 cc.kg−1.min−1, P < .001) and O2 delivery (29.2 ± 2.9 to 20.2 ± 1.6 cc.kg−1.min−1, P < .05). Addition of halothane decreased the critical level of O2 delivery from 17.9 to 14.3 cc.kg−1.min−1, but had no effect on the critical level of arterial Po2 (control group, 47 mmHg halothane, 46 mmHg). Peripheral oxygen utilization was mildly reduced during halothane anesthesia, as evidenced by a decrease in oxygen extraction (control group O2 extraction rate = 0.63; halothane group O2 extraction = 0.51, P < .05, unpaired t test). The reduction in critical DO2 suggests that halothane, by reducing tissue oxygen requirements, may be protective in hypoxemic patients.
Pediatric Research | 1987
Marc B. Hershenson; James A. Schena; Paul A Lozano; Robert K. Crone
Hypothermia (HT) has been used to reduce O2 consumption (VO2) in critically ill children. HT, however, does not reduce the critical level of PaO2 required to maintain VO2, because cardiac output (CO) and O2 extraction (O2 ext) are also decreased. We hypothesized that PENT, by increasing RBC deformability and vasodilation, would increase CO and O2 ext during HT, reducing the critical levels of O2 delivery (DO2) and PaO2. 15 adult beagles were exposed to hypoxic hypoxia during normothermia (38°C), HT (30°C) and PENT plus HT. We measured Hb, %sat, pO2, CO, blood viscosity and VO2, and calculated DO2 (CO·CaO2), SVR, PVR, O2 ext and critical DO2 and PaO2.Because of its effects on CO and O2 ext, HT alone did not reduce critical PaO2. PENT reversed HT-induced changes in CO and O2 ext without changing VO2, allowing reductions in critical DO2 and PaO2. When combined, PENT and HT reduce the susceptibility to hypoxia in dogs by reducing VO2 while maintaining DO2 and O2 ext. PENT and HT may be useful in severe, intractable hypoxemia.Supported by HL 07633.
Pediatric Research | 1985
James A. Schena; John E. Thompson; Marc B. Hershenson; Robert K. Crone; Allan W Walker
We describe a new apparatus for non-invasive measurement of VO2 in intubated children receiving high inspired oxygen concentrations. The apparatus is a modification of the closed circuit system originally described by Engstrom et al (Acta Anesth Scand, 1961). It consists of a standard Emerson 3PV Pediatric Ventilator enclosed in an airtight chamber in series with an Ohio 822 dry rolling seal spirometer, which is employed as a gas reservoir for the chamber. A circulating motor that supplies continuous flow of gas to the patient allows the system to measure VO2 during spontaneous ventilation. A CO2 adsorber is placed in the expiratory limb of the ventilator circuit to eliminate CO2 from the exhaled gas. Oxygen uptake by the patient results in a net volume loss within the chamber, which is then replenished by the reservoir gas contained in the spirometer, this gas volume equaling the patients VO2. We measured VO2 in 3 critically ill children who were receiving narcotics and muscle relaxants. After administration of morphine sulfate, VO2 (cc/kg/min) decreased from 5.0±0.1 to 2.9±0.5 (x ± SEM). Our technique for measuring VO2 may be useful in the management of nutritional and circulatory problems in critically ill children.
Pediatric Research | 1985
Mare B Hershenson; James A. Schena; Robert K. Crone; Allan W Walker
The effect of hypothermia on respiratory failure has not been studied. One possible advantage of hypothermia in respiratory failure is the reduction of cardiac output, which may in turn lower intrapulmonary shunting. We measured venous admixture and other cardiorespiratory variables in 5 anesthetized adult dogs before and after surface cooling to 30°C, and again after isovolemic hemodilution with Dextran 75. Arterial blood gases and hemoglobin saturations were corrected for temperature. Cardiac output was calculated from oxygen consumption, which was measured directly using a closed circuit method. Caridorespiratory variables measured at baseline (38°C), during hypothermia (30°C) and during hypothermia and hemodilution (30°C+H) are shown in the table below. (x ± SEM, *p<.05) Venous admixture fell dramatically in 4 out of 5 dogs (from .24 ± .05 to /08 ± .02, x SEM, p<.Ol).Hypothermia decreases intrapulmonary shunt in dogs and may be useful in patients with respiratory failure.
Pediatric Research | 1985
Marc B. Hershenson; James A. Schena; Robert K. Crone; Allan W Walker
Although hypothermia decreases cardiac output, oxygen consumption by the tissues is thought to decrease proportionately, so that tissue hypoxia does not occur. Hemodilution has been shown to increase cardiac output and tissue oxygenation. We hypothesize that hemodilution may be harmful by increasing cardiac output and oxygen need in excess of oxygen delivery. Oxygen consumption (V02) and arterial and venous blood gases were measured directly in 5 anesthetized dogs before and after cooling to 30°C and again after hemodilution (H) with Dextran 75. Cardiac index (CI), oxygen delivery (D02), oxygen extraction rate (02 ext) and oxygen equivalent (02 eq) were then calculated. Results are shown in the table below. (H=hemodilution, V02 units are cc/kg/min, *p<.05, ** p<.01).Although neither hypothermia nor hemodilution alone result in increased oxygen extraction, mild hypothermia and hemodilution together produce increased 02 extraction in order to avoid tissue hypoxia. It is possible that although hemodilution increased cardiac output, microvascular flow remained impaired necessitating increased oxygen extraction.
The New England Journal of Medicine | 1989
Benjamin L. Shneider; James A. Schena; Robert D. Truog; May S. Jacobson; Sherwin V. Kevy
Anesthesiology | 1990
Robert D. Truog; James A. Schena; Marc B. Hershenson; Babu V. Koka; Craig W. Lillehel
Journal of Applied Physiology | 1989
Marc B. Hershenson; James A. Schena; P. A. Lozano; M. J. Jacobson; Robert K. Crone
Anesthesiology | 1988
O. E. Mohan; Marc B. Hershenson; James A. Schena; Robert K. Crone