tailieunhanh - Critical Care Obstetrics part 47

Critical Care Obstetrics part 47 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 | Complications of Pre-eclampsia pre-eclamptic patients a lowered COP-PCWP gradient may have contributed to pulmonary edema 201 . From the foregoing discussion it is clear that non-hydrostatic factors pulmonary capillary leak and deceased COP may cause or contribute to pulmonary edema in patients with preeclampsia. In other patients highly elevated SVR may lead to decreased CO and LVSWI and secondary cardiogenic pulmonary edema. A similar hydrostatic pulmonary edema may have been seen with normal left ventricular function following iatrogenic fluid overload. The diagnosis of pulmonary edema is made on clinical grounds. Symptoms of dyspnea and chest discomfort are usually elicited. Tachypnea tachycardia and pulmonary rales are noted on examination. Chest X-ray and arterial blood gas analysis confirm the diagnosis. Other life-threatening conditions such as thromboembolism should be considered and ruled out as quickly as possible. Initial management of pulmonary edema includes oxygen administration and fluid restriction. A pulse oximeter should be placed so that oxygen saturation may be monitored continuously. A pulmonary artery catheter may be considered for severe preeclamptic patients who develop pulmonary edema antepartum in order to distinguish between fluid overload left ventricular dysfunction and non- hydrostatic pulmonary edema each of which may require different approaches to therapy. Furosemide Lasix 10-40mg IV over 1-2 minutes represents the first line of conventional therapy for patients with pulmonary edema associated with fluid overload. If adequate diuresis does not commence within 1 hour an 80- mg dose may be slowly administered to achieve diuresis. In severe cases of pulmonary edema a diuresis of 2-3 L needs to be achieved before oxygenation begins to improve. Again the degree of diuresis appropriate for these hemodynamically complex patients may be clarified by complete hemodynamic evaluation using parameters derived by a pulmonary artery catheter. An