New concepts about the pathophysiology of pulmonary edema

New concepts about the pathophysiology of pulmonary edema

LITERATURE REVIEW saphenous vein to 100% of its precontracted value. Papaverine was effective, but less potent, in coronary and mammary arteries cons...

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LITERATURE REVIEW

saphenous vein to 100% of its precontracted value. Papaverine was effective, but less potent, in coronary and mammary arteries constricted by potassium. The responses of the three vessels to calcium-entry blockers differed markedly. Saphenous veins were dilated almost maximally by nifedipine, verapamil, and diltiazem, with the greatest dilatation from nifedipine. Coronary arteries were also dilated by all calcium blockers, but verapamil was less potent in the artery than in the saphenous vein. Internal mammary arteries were resistant to dilatation by calcium blockers. Despite these differences, further work is required before an agent to prevent human vessel spasm can be suggested, although papaverine appears to be particularly effective in saphenous veins.

Hatazawa J, Ito M, Matsuzawa T, et al: Measurement of the ratio of cerebral oxygen consumption to glucose utilization by positron emission tomography: Its consistency with the values determined by the Kety-Schmidt method in normal volunteers. J Cereb Blood Flow and Metab 8:426-432,1988 Positron-emission tomography permits determinations of cerebral blood flow and cerebral metabolism. Its methodology differs completely from that of the KetySchmidt technique. In seven normal volunteers, cerebral blood flow was measured by having the subjects inhale 10 to 15 mCi/min of “O-labeled carbon dioxide. Oxygen extraction fraction was measured using inhalation of “O-labeled molecular oxygen 15 to 20 mCi/min continuously. The 2-deoxy-2-[‘*F] fluoro-D-glucose method was used to determine local cerebral metabolic rate for glucose (CMRGlc). Combination of these techniques permits evaluation of regional changes in the metabolic ratio of oxygen given to glucose. In the cortical gray matter, the CMRO,/CMRGlc ratio was 4.89. Similar values were found in both basal ganglia and white matter (5.27 and 5.82 respectively), indicating the presence of similar oxidative glucose metabolism. For the whole brain, the Kety-Schmidt derived ratio is 5.5. PET requires various model parameters and analytical methods not requisite to the Kety-Schmidt technique. Low spatial resolution in present-generation positron tomography probably accounts for the 10% inaccuracy compared to the KetySchmidt technique in estimating CMROJCMRGlc ratio in gray matter.

Staub NC: New concepts about the pathophysiology of pulmonary edema. J Thorac Imaging 3%14,1988 This paper is part of a symposium issue on pulmonary edema in this journal. Three major concepts are presented. First, the microvascular filtration surface area is as important as the microvascular hemodynamic state determined by pulmonary artery and pulmonary venous pressures and resistances in assessing lung filtration. Filtration surface area is increased by exercise and other hemodynamic changes. A second concept is the difference in clearance of protein and electrolytes from the lung. Clearance of electro-

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lytes from the lung proceeds quickly (half-life four hours), probably by active metabolic transport across alveolar epithelium. Protein leaves alveoli at a much slower rate, probably by transcytosis across the alveolar epithelium. Protein is not degraded or cleared by alveolar macrophages. Alveolar liquid clearance is enhanced by beta-adrenergic agonists. Finally, although the major pathway for clearance of lung liquid is via the lymphatics, the mediastinum and pleural spaces may also be important. Using a fiberoptic bronchoscope to inject radioactive albumin into bronchovascular edema cuffs in sheep, the author found radioactivity in the mediastinum. Of the factors affecting transvascular filtration in the lung, the clearance pathways are the most important in the prevention of pulmonary edema.

Scalea TM, Holman M, Fuortes M, et ah Central venous blood oxygen saturation: An early, accurate measurement of volume during hemorrhage. J Trauma 28:725-732,1988 Measurement of blood volume is not a readily available test and fails to provide continuous information for patient care. Attempts to monitor blood volume using cardiovascular parameters are often misleading, since patients may exhibit normal blood pressure and heart rate even after significant blood loss. Sixteen mongrel dogs were hemorrhaged 24% of total blood volume during thiopental anesthesia. Systolic, pulse, mean arterial, wedge, and central venous pressures were observed during incremental hemorrhage (3% of blood volume). Mixed venous oxygen saturation and central venous oxygen saturation (in unanesthetized animals) were also measured. Mixed venous oxygen saturation decreased after removal of 3% to 6% of blood volume. The mean correlation coefficient relating blood volume to mixed venous oxygen saturation was 0.94. This value was 0.92 for central venous oxygen saturation. However, in one animal there was no correlation between blood loss and central venous oxygen saturation. Cardiac index also decreased linearly with blood volume, with a correlation of 0.85. Poor correlations of blood volume with heart rate and pulse pressure were noted. However, additional studies in humans are necessary to validate the method and to assess whether knowledge of oxygen saturation alters patient outcome.

Marder VJ, Sherry S: Thrombolytic therapy: Current status (parts I and II) N Engl J Med 318:1512-1520 and 1585-1594,1988 The sites of action, pharmacology of the available thrombolytic agents (doses, duration infusions, fibrin specificity, half life), factors affecting reperfusion (timing of administration), and complications are detailed in this twopart review. Plasminogen activators achieve both vascular reperfusion and hemorrhagic complications by degradation of fibrin in pathologic thrombi as well as hemostatic plugs. Plasmin-induced lysis of other adhesive proteins causes platelet disaggregation. Vascular injury, rather than the changes in coagulation, may be the primary cause of bleeding after thrombolytic therapy. Evidence for this view includes the poor correlation between the extent of hypofibrinogenemia