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Critical Care Obstetrics part 37

Critical Care Obstetrics part 37 provides expert clinical guidance throughout on how you can maximize the chances of your patient and her baby surviving trauma. In this stimulating text, internationally recognized experts guide you through the most challenging situations you as an obstetrician are likely to face, enabling you to skillfully:Recognize conditions early-on which might prove life threatening, Implement immediate life-saving treatments in emergency situations, Maximize the survival prospects of both the mother and her fetus | Pulmonary Edema Table 25.1 Clinical setting of pulmonary edema in pregnancy. Tocolytic therapy Pre-eclampsia eclampsia Cardiac disease Obesity chronic hypertension diastolic dysfunction Sepsis acute lung injury Thyroid storm Renal failure Profound anemia Acute myocardial infarction Intravenous heroin Intracranial hemorrhage Amniotic fluid embolism Multifactorial pressure increase. There is a redistribution of intravascular volume from the systemic circulation to the pulmonary circulation resulting in alveolar flooding. With backward failure of the right heart there is decreased emptying of the right ventricle and elevated central venous pressure CVP resulting in peripheral edema neck vein distension hepatojugular reflux hepatic congestion and jaundice. Clinical manifestations of forward failure result from an inadequate discharge of blood into the arterial system. If left ventricular forward output is decreased blood pressure falls. The kidneys sense decreased effective blood volume and increase renin angiotensin and aldosterone production resulting in salt and water retention and increased systemic vascular resistance SVR . With forward failure of the right heart there is an interventricular septal shift to the left compromising the left ventricular cavity and decreasing stroke volume. This results in increased left ventricular filling pressure decreased blood flow through the lungs Figure 25.1 Schematic representation of alveolar epithelial cells types I and II depicting the apical Na channels the basolaterally located Na K-ATPase the aquaporins AQPs and some of the cotransporters. Sodium enters through the apical membrane via Na channels and is extruded by the Na K-ATPase with water following isosmotically Also shown is an airway epithelial cell with associated basolateral aquaporins. Reproduced by permission of the publisher Springer-Verlag from Dematte JE Sznajder JI. Mechanisms of pulmonary edema clearance from basic research to clinical implication. .