病理生理学-呼吸系统技术方案.pptVIP

respiratory failure ( respiratory insufficiency ( ) restrictive hypoventilation ( ) obstructive hypoventilation ( ) diffusion impairment ( ) functional shunt ( ) venous admixture ( ) anatomic shunt ( ); true shunt( ) dead space like ventilation ( ) ventilation-perfusion ratio ( ) acute respiratory distress syndrome (ARDS) ( ) cor pulmonale ( ) pulmonary encephalopathy ( ) Congestive Heart Failure and Pulmonary Edema Pathophysiology: CHF is summarized best as an imbalance in Starling forces or an imbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in an ensuing contraction. This imbalance may be characterized as a malfunction between the mechanisms that keep the interstitium and alveoli dry and the opposing forces that are responsible for fluid transfer to the interstitium. Maintenance of plasma oncotic pressure (generally about 25 mm Hg) higher than pulmonary capillary pressure (about 7-12 mm Hg), maintenance of connective tissue and cellular barriers relatively impermeable to plasma proteins, and maintenance of an extensive lymphatic system are the mechanisms that keep the interstitium and alveoli dry. Opposing forces responsible for fluid transfer to the interstitium include pulmonary capillary pressure and plasma oncotic pressure. Under normal circumstances, when fluid is transferred into the lung interstitium with increased lymphatic flow, no increase in interstitial volume occurs. When the capacity of lymphatic drainage is exceeded, however, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung vasculature, thus creating CHF. When increased fluid and pressure cause tracking into the interstitial space around the alveoli and disruption of alveolar membrane junctions, fluid floods the alveoli and leads to pulmonary edema. Etiologies of pulmonary edema may be placed in the following 6 categories: Pulmonary edema secondary to altered capillary permeability: This categ