This short article is one of ten reviews selected from your

This short article is one of ten reviews selected from your Yearbook of Intensive Care and Emergency Medicine 2010 (Springer Verlag) and co-published as a series in Critical Care. reduction in venous return induced by positive intrathoracic pressure at each insufflation [1]. By contrast positive pressure air flow exerts beneficial effects in individuals with cardiogenic pulmonary edema such that it is definitely routinely used like a therapy with this category of individuals [2 3 Conversely cardiac effects of spontaneous deep breathing may be responsible for weaning failure in individuals with remaining heart disease even though the mechanical air flow was required for respiratory failure of noncardiac source. Since its 1st description more than twenty years ago [4] cardiogenic pulmonary edema has been recognized as a frequent cause of weaning failure in individuals with underlying remaining cardiac dysfunction. With this chapter we 1st briefly summarize the mechanisms by which pulmonary edema can develop during weaning. We then emphasize how weaning failure of cardiac source can be recognized in the bedside since significant progress has recently been made in this field. Finally we describe the restorative options currently available. Mechanisms contributing to the development of weaning-induced pulmonary edema The mechanisms that contribute Rabbit Polyclonal to OR5AS1. to development of cardiogenic pulmonary edema during weaning have been extensively detailed inside a earlier review [5]. These mechanisms are complex and mainly Calcipotriol include the inspiratory fall in intrathoracic pressure the increase in work of deep breathing and the catecholamine discharge that happen during abrupt transfer from mechanical air flow to spontaneous deep breathing [5]. Inspiratory fall in intrathoracic pressure tends to increase the systemic venous return Calcipotriol pressure gradient and the central blood volume [5] and to decrease the remaining ventricular (LV) ejection pressure gradient having a resulting increase in LV afterload [5]. A designated increase in work of deep breathing may increase cardiac work and myocardial oxygen demand [5]. The improved adrenergic tone may also increase venous return LV afterload cardiac work and myocardial oxygen demand and may thus potentially result in myocardial ischemia in predisposed individuals [4 6 In individuals with pre-existing right ventricular (RV) disease an increase in weaning-induced RV afterload may occur because of hypoxemia or worsening of intrinsic positive end-expiratory pressure (PEEPi) [5]. In addition to the simultaneous increase in systemic venous return the improved RV afterload may lead to a designated RV enlargement during weaning therefore impeding the diastolic filling of the remaining ventricle through a biventricular interdependence mechanism [5]. In summary elevation of the LV filling pressure can occur during weaning because of an increase in LV preload and/or decrease in LV compliance (myocardial ischemia biventricular interdependence) and/or increase in LV afterload. However in the absence of remaining heart disease the rise in pulmonary artery occlusion pressure (PAOP) is limited [7 8 In Calcipotriol contrast designated raises in PAOP have been reported to occur during unsuccessful weaning in individuals with remaining heart disease [4 9 who can thus become suspected to have failed to wean because of the onset of cardiogenic pulmonary edema. Analysis of weaning-induced pulmonary edema Clinical context The analysis of weaning-induced pulmonary edema should be suspected when intolerance to a spontaneous breathing trial (SBT) happens and other causes of weaning failure have been discarded. The suspicion is definitely reinforced by the fact that the patient Calcipotriol has a earlier history of remaining heart disease. Patients with a combination of remaining heart disease and chronic obstructive pulmonary disease (COPD) are at higher risk of weaning-induced pulmonary edema. In this situation the increase in airway resistance amplifies two mechanisms responsible for LV filling pressure elevation: 1) the fall in intrathoracic pressure is definitely exaggerated at inspiration leading to a designated increase in LV afterload during spontaneous deep breathing; and 2) the work of deep breathing further augments leading to increased myocardial oxygen demand with inherent risks of myocardial ischemia in predisposed individuals. In addition the biventricular interdependence trend.