Question

Mr. Smith, a 77-year-old man who was admitted to the intensive care unit (ICU) post- surgery for peritonitis following a perforated colon. Due to your superior intellect nursing skills over the course of a few days, he is stabilized and recovering from sepsis. You are now attempting to wean him off of the ventilator. Questions 1. Describe briefly what you know about the pathophysiology of ARDS and risk factors. Unfortunately, on his way home from the hospital he hits a tree and sustains blunt chest trauma. A chest tube was inserted in the ER to treat a pneumothorax and hemothorax. Although he is in a lot of pain, he is ecstatic to have you as his nurse again. You note that the drainage system has drained 400ml of light red fluid in the first 6hrs after insertion. The patient is becoming increasingly anxious and SOB during the past hour. Questions What do you anticipate to be potential causes of his acute onset SOB at this 1. time? What are you going to do first and why?

Answer 1

While it is not clear who will develop ARDS, there are a few factors that may increase the risk for ARDS. These factors include:

• A history of cigarette smoking
• Oxygen use for a pre-existing lung condition
• Recent high-risk surgery
• Obesity
• Low protein in the blood
• Alcohol abuse
• Recent chemotherapy

The pathophysiology of the acute respiratory distress syndrome (ARDS) is characterized by pulmonary edema, decreased lung compliance and profound arterial hypoxemia. The syndrome has several apparent `triggers' and involves several cell types, most notably microvascular endothelial cells and polymorphonuclear leukocytes or neutrophils. These cells interact through several classes of adhesive determinants on both the endothelial cell and neutrophil which govern leukocyte binding, transendothelial migration and the extent of injury to the lung. The lung injury elicited by leukocytes involves the release of several mediators which include oxidants and proteases, of which elastase now appears to be the most important in pulmonary injury. There are several potential targets of oxidants and proteases in the lung which include the endothelial cell membrane, glycocalyx and basement membraneas well as endothelial and epithelial junctional proteins. Destruction of these elements appears to be responsible for increased pulmonary microvascular permeability and lung edema formation and may also facilitate neutrophil-transendothelial migration. This review focuses on the structure and function of the alveolar-capillary membrane and the forces that govern leukocyte trafficking in the lungs as a background to understanding the pathophysiology of lung injury in ARDS.