Concerns over the quality of this blood and its effect on outcome of CPB have lead manufacturers to produce software with a separate cardiotomy reservoir which allows cardiotomy blood to be kept from the systemic circulation. The valve which holds the blood in the cardiotomy has a central lumen and a luer connection allowing the stored blood to be discarded or treated in some way. (e.g. Dideco D903 Avant)
The drop in perfusion pressure when pleural blood is aspirated into the cardiotomy during CPB is well documented. This has been shown by Singh and Lavee in most part to be due to prostacyclin.
However it was noticed that when blood aspirated from the left heart vent in this case from the aortic root, was stored in the cardiotomy and added to the systemic circulation as a bolus there was also a drop in pressure, and the effect was repeatable.
One possible explanation is that increased blood damage caused by the suction leads to increased levels of cytokines. Cytokines increase cellular expression of inducible nitric oxide synthase, thus increasing cellular production of nitric oxide, a known inflammatory mediator and potent vasodilator. Reents et al from Wurzburg, Germany published evidence that showed increased levels of proinflammatory cytokines in cardiotomy suction blood.
So what!
The most quoted negative effect of CPB is post-operative neurological sequelae. The incidence of major and minor deficits may be as high as 60 - 80%. Aetiology of many of these deficits, which range from overt stroke to subtle neuropsychological changes, such as behavioural, intellectual, and fine motor disturbances, is at least partly caused by arterial embolisation. While overt stroke is caused by gross atherosclerotic emboli, the less severe neurological deficit appears to be related to microscopic debris.
Microdebris includes air, cellular fragments, silicone particulates have all been associtaed with cardiotomy suction.
Autopsy studies in patients after CPB have shown microsopic emboli, composed primarily of lipid, within the microvasculature of the brain. When stained they show as small capillary and arteriolar dilatations or SCADS. They are detected in the brain after CPB and range in size from 10 to 70 microns.
While the exact source of these are unknown studies as early as 1974 demonstrate a direct relationship between the use of cardiotomy suction and the production of microemboli. More recently Brooker and co-workers, in a canine model, demonstarted SCADS after the use of left heart bypass with cardiotomy suction, but not with right heart bypass or without cardiotmy suction.
Kincaid showed that the incidence of SCADS is reduced by processing the Cardiotomy blood with the continuous cell washer CATS system.
Workers are still not 100% sure where the fat is coming from. It could be part of the inflammatory process but it sems more likely that it comes from the fat surrounding the heart or chest wall that is disturbed by the surgery itself.
There is still no link between SCADS and neurological dysfunction following CPB but common sense tells us that outcome must be effected.
References:
1. Lavee J, Naveh N, et al. J Thorac Cardiovasc Surg 1990;100:546-51
2. Singh H, Coleman E. Ann Thorac Surg 1995;59:647-50
3. Reents W et al. Ann Thorac Surg 1999;68:58-62
4. Shaw PJ, Bates D, et al. Quart J Med 1986;58:59-68
5. Treasure T, Smith PL et al. Eur J Cardiothorac Surg 1989;3:216-21
6. Sylivris S, Levi C et al. Ann Thorac Surg 1998;66:1674-8
7. Brooker RF, Brown WR et al. Ann Thorac Surg 1998 Jun;65(6):1651-5
8. Kincaid EH, Jones TJ. Ann Thorac Surg 2000;70:1296-300