Gaseous microemboli and hyperoxia.
نویسنده
چکیده
A recent issue of JECT contained two articles on air bubbles in the cardiopulmonary bypass (CPB) circuit and an article on the routine use of hyperoxia during CPB (1–3). Interestingly, these two subjects are related in a way that perfusionists do not commonly associate. The article by Dickinson et al. (1) and the commentary by Willcox and Mitchell (2) suggested that gaseous emboli passing to the patient from a CPB circuit are, for some patients, inevitable. Some circuits are better than others at removing the potential emboli, but no circuit is 100% safe. The general advice of these authors is to play it safe by preventing air entrainment into the circuit to minimize the potential for gaseous emboli. In other words, nag the surgeon when air bubbles are streaming down the venous line or when the suckers and vent are pumping air-emulsified blood into the cardiotomy reservoir and hope that solves the problem. How dangerous are these gaseous microemboli (GME)? Recent work by Floyd et al. (4) showed that patients undergoing real “open heart” procedures such as valve replacements and aortic arch reconstructions, wherein air entrainment through the venous line, vent, or suckers is a much greater possibility, have silent (asymptomatic) brain infarcts 18% of the time in addition to the 1.5%–10% of patients who have obvious strokes. The long-term sequelae from these silent infarcts is unknown. What options does the perfusionist have when confronted with air entrainment? One option is to slow down the pump speed to give bubbles more time to rise in the venous reservoir. But, is this a practical choice? For option 2, volume can be added to the venous reservoir to decrease vortexing. The extra volume also increases the bottom pressure to improve bubble buoyancy. This works for big bubbles, but very small air bubbles have very little positive buoyancy and are much more influenced by fluid current. Once the air bubbles enter the patient’s circulation, the only practical option left is “off-gassing.” Offgassing is the treatment for the bends and is the most effective means of removing nitrogen-filled GMEs from a patient’s body. Patients with the bends are usually divers. However, iatrogenic injection of air as GMEs or as gross air embolus as might occur in open heart patients would also qualify as having the bends. Off-gassing usually involves two steps for the patient suffering from the bends. The first, and most important step, is to stop breathing nitrogen-filled air and breathe only 100% oxygen. In the patient who is on CPB, this means using a sweep gas of 100% oxygen. The high concentration of oxygen in the arterial blood does two things. 1) Any nitrogen in the bubbles passing through the oxygenator will quickly off-gas and be replaced by oxygen. If an oxygen bubble passes on into the patient in the form of a GME and obstructs a vital arteriole or capillary, the oxygen will be quickly absorbed and the blockage removed. 2) The high blood PaO2 and low PaN2 will quickly off-gas nitrogen from the body tissues. Nitrogen bubbles already trapped in arterioles and capillaries will be removed 10 times faster if 100% oxygen is used compared with room air (5). CPB procedures are usually long enough that nitrogen emboli passed to the patient at the beginning of a case can be entirely removed by the end of the case if the alert perfusionist began using 100% oxygen early. The second step for treating nitrogen bubbles in the blood requires recompression to at least three atmospheres of pressure. This is not practical with a patient on CPB. However, Figure 1, from the U.S. Navy Decompression Table 5, shows the tolerance humans have for high levels of oxygen. Intermittent breathing of room air for short periods (the “oxygen clock” theory) reduces the stress on antioxidant enzymes that control reactive oxygen species (ROS). It also prevents excessive “on-gassing” of nitrogen during the decompression stages. This intermittent breathing of room air reduces the potential for oxygen toxicity, which is often confused with ischemic reperfusion injury. Oxygen toxicity occurs when the amount of oxygen present exceeds the antioxidant enzymes’ ability to control the production of ROS, whereas the tissue pH remains normal because of the fact that there is no ischemia (6). Oxygen toxicity takes many hours or even days to develop. In ischemic reperfusion injury, JECT. 2006;38:367–369 The Journal of The American Society of Extra-Corporeal Technology
منابع مشابه
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ورودعنوان ژورنال:
- The journal of extra-corporeal technology
دوره 38 4 شماره
صفحات -
تاریخ انتشار 2006