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R C Schaeffer

Publications and source records attributed to R C Schaeffer.

47 records · Page 3Linked to original sources
PubMed1976

Oxygen transport during extracorporeal oxygenation for the treatment of adult respiratory distress syndrome.

An inventory of hemodynamic and respiratory measurements was obtained in two patients with acute respiratory failure syndrome prior to and during venoarterial extracorporeal membrane oxygenation for study of oxygen transport. As the inspired oxygen concentration fraction was reduced from 1.0 to 0.5 and paO2 was increased from less than 50 to physiologic ranges during extracorporeal membrane oxygenation, tachycardia and pulmonary hypertension were reversed. Total oxygen transport was reduced rather than increased. Oxygen consumption and oxygen extraction were not altered during extracorporeal membrane oxygenation. However, a striking reduction was observed in cardiac output. After reversal of anoxemia, the total of the cardiac output of the patient and the extracorporeal membrane oxygenation flow were less than the cardiac output of the patient prior to extracorporeal membrane oxygenation. These observations provide evidence that the beneficial effects of extracorporeal membrane oxygenation stem, at least in part, from a reduction of the work load on the heart. Since high cardiac output failure is observed during progression of adult respiratory distress syndrome, mechanical support of circulation during extracorporeal membrane oxygenation may be of primary therapeutic benefit.

Adult↗
PubMed1975

Rattlesnake venom shock in the rat: development of a method.

A model in Wistar rats (n = 30, 279-345 g) was developed to study circulatory, respiratory, metabolic, and lethal effects of an intravenous infusion (30 min; 1.25, 1.5, 1.75, and 2.0 mg/kg) of rattlesnake (Crotalus viridis helleri) venom. Venom produced perfusion failure with lactacidemia, hemoconcentration, hypoproteinemia, and death. The severity of poisoning was proportional to the quantity of venom given and to the elevation in lactic acid and hematocrit. Hemorrhages in the diaphragm, intercostal muscles, and intestine were observed at necropsy. In a separate test, rats (n = 12, 311-355 g) received an infusion of 1.5 mg/kg of venom or physiological salt solution. Blood volume was measured 30 min after the end of infusion in both groups with radioiodinated (125I) human serum albumin (RIHSA) and 51Cr-labeled rat red cells. Venom produced a significant reduction in total blood volume index (35%, P less than 0.001), plasma volume index (46%, P less than 0.001), and red cell mass indec (22% P less than 0.005). The slope of the RIHSA-disappearance curve of animals that received venom was more than twice that of the control group. We conclude that perfusion failure following rattlesnake envenomation is associated with hypovolemia due to increases in vascular permeabiltiy and hemorrhage.

Animals↗
PubMedDate not supplied

Pichinde virus-induced respiratory failure due to obstruction of the small airways: structure and function.

Respiratory distress that leads to death is seen in patients with Lassa fever. The development of this respiratory problem was studied using a Pichinde virus model (10(4) plaque forming units, IP, survival time 20 +/- 1 days) in strain 13 guinea pigs (n = 35, 229-353 g) of this lethal human contagious infectious disease. Extravascular lung water to bloodless dry lung weight (EVLW/BDLW) ratio showed a modest yet significant increase in animals 13 and 18-21 days postinoculation (PI). In contrast, residual lung blood and lung radioactive 125I-labeled human serum albumin activity index were elevated only in the 18- to 21-day group. These data are consistent with the progressive severity of perivascular edema, lymphocytic pneumonitis, and some alveolar protein between days 13 and 18-21 PI. Lymphocytic pneumonitis appeared to be distributed near most airways and was proportional to the degree of Pichinde virus antigen staining of alveolar macrophages, large mononuclear cells within the pulmonary vascular and extravascular spaces, and alveolar-capillary membranes. These findings suggest that lymphocyte recruitment to the lung reflects the Pichinde virus-induced cell-mediated immune response. Obstructed small bronchi with some lumenal cell debris and hypertrophied epithelial cells were found associated with the areas of marked pneumonitis. The severe hypoxemia and modest anaerobic metabolism in association with marked tachypnea and normocapnia are consistent with small airway obstruction and wasted ventilation, since no change in arterial blood pressure, heart rate, hematocrit, hemoglobin, or blood volume was noted. These data suggest that Pichinde virus-induced respiratory failure was due to obstruction of the small airways with wasted ventilation in association with lymphocytic pneumonitis.

Airway Obstruction↗