Jan D. Smith

Thromboelastography used to assess coagulation during treatment with molecular adsorbent recirculating system

Abstract:  Coagulopathy is a life‐threatening complication of liver cirrhosis. We describe the effect of molecular adsorbent recirculating system (MARS), a cell‐free dialysis technique, on the blood coagulation of cirrhotic patients.

Intrathoracic pressure, pulmonary vascular pressures and gas exchange during pulmonary lavage

Intrathoracic pressure, blood pressures of intrathoracic vascular structures (central venous, mean pulmonary arterial, pulmonary- “capillary” (wedge) and left ventricular end-diastolic pressures) and Para were measured as a function of pulmonary lavage in a patient, three dogs and a calf. Instillation of liquid in a single lung leads to an increase in intrathoracic pressure generated by the hydrostatic pressure of the liquid column used fur instilling the liquid. The blood pressures of intrathoracically located vessels increase as a result of the increased intrathoracic pressure und as a result of an acute mediastinal shift away from the liquid-filled lung. There is loss of perfusion to liquid-filled alveoli because of increased alveolar pressure. As a result, Pao2 is increased, since pulmonary blood flow is shifted to non-liquid-filled (ventilated) alveoli. Drainage of the lung causes a reduction of Pao2 because of restoration of perfusion to nonventilated (collapsed) alveoli.

Ion and macromolecular transport in the alveolar macrophage

Abstract 1. 1. Some aspects of Na+, K+, Cl− and macromolecular transport have been studied in isolated rabbit alveolar macrophages. Steady-state intracellular concentrations in Ringers solution (pH 7.4) were as follows: Na+, 83 ± 7.1 (S.E.); K+, 75 ± 13.2 ; Cl, 59 ± 4.1 mequiv/kg cell water. Cl− is rapidly and completely lost from the cell in Cl−-free media suggesting rapid thermodynamic equilibrium between intracellular and extracellular phases. 2. 2. Na+ efflux has two rate constants (rapid phase 636 ± 302 (S.D.); slow phase 329 ± 125 mequiv/kg cell water per h). It appears that this cell has high permeability for Na+ and the high leak down the electrochemical gradient requires a high rate of active transport. Thermodynamic considerations suggest that the major energy source for active Na+ transport is derived from oxidative phosphorylation. 3. 3. Classical relatively high molecular weight extracellular markers are excluded from cell water. However, ferritin (mol. wt. 465000) influx is rapid with intracellular/extracellular concentrations greater than 1.0 within 3 min. Ferritin efflux is exceedingly slow so that there is essentially unidirectional transport. Simultaneous exposure of cells to both ferritin and dextran leads to no measurable increase in cellular dextran uptake suggesting high specificity for ferritin uptake.

Problems in brain death determination

During the last decade there has been philosophical acceptance of the concept that the state of brain death is equivalent to total patient death. The application of this concept to clinical medicine has been associated with major problems in both the diagnosis of brain death and the medical management of the brain dead patient. In our experience with 176 consecutive cases of suspected brain death over a seven-year period, we have found that a standardized protocol applied by experienced clinicians will minimize these problems.

Need for Oxygen Enrichment in Myogardial Infarction, Shock and Following Cardiac Arrest

The abundance of data of the systemic circulation in various types of shock and following cardiac arrest is contrasted by a surprising lack of information on pulmonary changes. We have seen hypoxemia in most patients with clinically reduced cardiovascular function, calling for respiratory care. Maximal arterial oxygen content is needed for maintaining oxygen delivery to tissues in conditions of reduced blood flow. Universal acceptance of exhaled-air ventilation and bag-mask-air ventilation has created the impression that oxygen enrichment is not required. The observations by others and ourselves to be reported indicate that an early switch to ventilation with increased oxygen concentrations is called for. We like to define shock as “the clinical picture of inadequate total tissue perfusion.” The pathogeneses are based on one or a combination of the following: (1) oligemia; (2) systemic vasodilation; (3) pump failure (reduced cardiac contractility); and (4) increased pulmonary vascular resistance from embolization or spasm. Any one of these factors may lead to a vicious cycle of metabolic acidosis, cardiac failure, refractory hypotension and irreversible tissue damage. The management of shock states must support oxygen transport to the organism, and not merely arterial pressure (Tabel 1). Oxygen transport (oxygen delivery, oxygen availability) equals blood flow times arterial oxygen content. The normal 70 kg resting adult thus has about 1 liter of oxygen per minute supplied to his systemic capillaries with a cardiac output of about 5 liters per minute and an arterial oxygen content of about 20 volumes percent. 250 ml of oxygen are used for metabolism under resting conditions. A reduction of oxygen delivery to the capillary bed may be the result of decreased blood flow, loss of hemoglobin and/or

Noncardiogenic pulmonary edema induced by a molecular adsorbent recirculating system : case report

Noncardiogenic pulmonary edema is a well-recognized manifestation of acute lung injury which has been related, among others, to blood or blood-product transfusion, intravenous contrast injection, air embolism, and drug ingestion. We describe two cases of noncardiogenic pulmonary edema after use of a molecular adsorbent recirculating system, a cell-free dialysis technique. Patients in this series presented at our institution to be evaluated for liver transplantation. Subsequently, they developed an indication for the molecular adsorbent recirculating system. Two patients of 30 (6.6%) treated with the molecular adsorbent recirculating system for acute-on-chronic liver failure and intractable pruritus had normal chest X-rays before treatment and developed severe pulmonary edema, in the absence of cardiogenic causes, following use of the molecular adsorbent recirculating system. For each patient we reviewed the history of blood or blood-product transfusion, echocardiograms if available, daily chest X-rays, and when available pre- and postmolecular adsorbent recirculating systemic blood pressure, central venous pressure, pulmonary arterial pressures, cardiac output, cardiac index, systemic vascular resistance index, and arterial blood gas. Our data suggest that the molecular adsorbent recirculating system may cause noncardiogenic pulmonary edema, possibly by an immune-mediated mechanism.

Cation transport and energy metabolism in the high Na+, low K+ erythrocyte of the harbor seal, Phoca vitulina.

1. 1. Cation transport in relation to cell metabolism in the high Na+, low K+ seal erythrocyte was investigated. Under steady-state conditions at 40°C, Na+ efflux was32 ± 4·0 (S.D.) m-equiv. × kg RBC H2O−1 × hr−1and K+ influx was 1·1 ± 0·38m-equiv. × kg RBC H2O−1 × hr−1. 2. 2. Both fluxes were insensitive to ouabain (10−4 M) and an inhibitor of anaerobic metabolism, monoiodoacetate (10−4 M). 3. 3. Ethanol (5 × 10−1 M) decreased Na+ efflux in the seal erythrocyte and the high Na+, low K+ cat erythrocyte but did not affect Na+ transport in the low Na+, high K+ human erythrocyte. 4. 4. Valinomycin (10−5 M) produced increased permeability to K+ without effect on Na+ transport. 5. 5. Lactate production (2·4 ± 0·29 mM×1.RBC H2O−1 × hr−1) was not decreased significantly by ouabain. 6. 6. Adenosinetriphosphate (ATP) concentrations (0·4 ± 0·03 (S.D.)mM/5·0 mM Hb) and 2,3 diphosphoglycerate (2,3 DPG) concentrations (6·5 ± 0·53 (S.D.) mM/5·0 mM Hb) provide evidence that this cell possesses an active glycolytic mechanism for high energy phosphate production. 7. 7. Quantitatively, the level of energy transduction is similar in both high Na+, low K+ seal erythrocytes and low Na+, high K+ human erythrocytes despite the small calculated minimal work cost of cation transport in the former.

Sauerstofftransport nach Herz-Lungen-Wiederbelebung

Hypoxamie, Hyperkapnie und metabolische Acidose werden haufig nach Herz-Lungen-Wiederbelebung beobachtet [3, 5, 6]. Die hier berichteten Ergebnisse an Patienten und im Tierexperiment zeigen, das die Acidose mit Natriumbikarbonat und Hyperkapnie durch Beatmung korrigiert werden konnen. Die Therapie der Hypoxamie ist jedoch oft problematisch.