Systemic embolism affecting the brain is a recognized complication of Cardiopulmonary bypass (CPB); Focal neurological deficit has been associated secondary to gaseous embolism or hypoperfusion by particulate microemboli. Also compelling evidence of link between microemboli and poor neurological outcomes have been found when the number of detected emboli is directly compared with patients undergoing same surgical procedures. There have been extraordinary improvements in clinical practice through ongoing research and development, improvements in technology, equipment, techniques and management of CPB have minimized major complications that were faced in early days; however, microemboli generation remains the fact of CPB use.
Cardiopulmonary bypass circuit (CPB) is composed of an oxygenator, venous reservoir, arterial filter, PVC and Silicone tubing. During a CPB blood is drained by gravity into venous reservoir via cannulae placed in right atrium, then blood is forced through an oxygenator by a pump into a cannula placed in the aorta. Along this transition, blood is exposed to the artificial surfaces of oxygenator, reservoir, tubing, filters etc, as well as other non physiological condition which are places for microemboli creation. Humoral and cellular components of blood are also activated, these not only include the coagulation system, but kallikrein-kinin, fibrinolytic, release of cytokines and production of oxygen-free radicals. This surface contact also activates arachidonic acid metabolites, platelet activating factor (PAF), nitric oxide (NO), endothelins, complement systems, platelets and leukocytes which are found to be basis of microembolic damage. Furthermore, these systems have a capacity to cross-activate one another and cause a systemic response and embolization. Due to the contact of blood with non-biological surfaces, cardiopulmonary bypass (CPB) induces a whole body response and increases postoperative morbidity and mortality directly related to bleeding complications and end organ dysfunction due to microemboli creation. Normally blood circulates within a vascular system; it is in contact with endothelial cell layers capable of producing, secreting and binding anticoagulants and pro-coagulant factors. This maintains blood fluidity and vascular integrity. However, with CPB circuit blood comes in contact with outside environment and loses this balance. Furthermore, gaseous microemboli have been long associated with CPB, due to the nature of complexity and circuit design. There are various sources in CPB circuit where generation of emboli occurs, oxygenators, venous reservoirs, cardiotomy suckers, intracardiac vents are some of them. Both roller pumps and centrifugal pumps produce negative pressures when venous inflow is obstructed, pinholes in tubing, cracked connectors, incompletely closed stopcocks and poorly tight catheter ligatures are some of the ways microemboli are generated throughout the CPB circuit.
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An embolus can be defined as deformable (conformal) or non deformable (particulate) gaseous or solid particles that obstruct circulation to arterioles, pre capillaries, and venules, which range from 6 to 40Âµm in diameter. The body contains a huge number of micro-vessels; in cross-sectional are the capillary bed is estimated to be 800 times that of an aorta. As the arterial tree subdivides, myriads of branches are formed so that the number of branches 40Âµm or less in diameter is incalculable. For microemboli to cause detectable organ damage, thousands perhaps millions of arterioles, pre-capillaries and capillaries must be obstructed. Extracorporeal perfusion systems have long been recognised to produce the vast number of microemboli needed to produce end organ damage from occlusion of the microcirculation; however , more damage can be caused by fewer emboli if the emboli are larger than 35 to 40Âµm. These large emboli obstruct small arteries and large arterioles and thus stop circulation to organ and tissue segments before these vessels arborize into the microvasculature; axiomatically, the larger the embolus, the larger the segment of an organ or tissue rendered ischemic.
Embolism is a well known cause of cardiopulmonary bypass (CPB) mortality and morbidity, as emboli in arterial vessels cause symptoms of end-artery obstruction, tissue ischemia and necrosis. The brain is particularly susceptible to embolic damage, leading to many reports of poor neurological outcomes following CPB. It has been demonstrated that within first week after coronary artery bypass surgery using CPB, up to 83% of all patients demonstrated a degree of cognitive dysfunction and 35% exhibited neurophysiological dysfunction at 5years follow. Also for patients undergoing open chamber procedures (e.g., valve surgery) neurologic injury or frank stroke was apparent in 4.3% to 13% of patients, which has been linked to risk of embolization, hemodynamic instability and pro-long cardiopulmonary bypass time.
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Emboli can generally be differentiated on the basis of size and composition; such a distinction may also reflect different clinical manifestation. Emboli which are greater than 200Âµm can occlude flow in arteries and are called macroemboli. A single macroemboli can occlude artery and may be the cause of hemiplegia, but a solitary microemboli usually smaller then 200Âµm is unlikely to have a noticeable effect except in very susceptible tissue such as retina. On the basis of composition emboli can be gaseous, particulate debris of various composition and biological material. A lipid droplet or microgaseous bubble will change shape to stick and slip as it progresses through the vessel, dividing into smaller units to eventually pass through capillary bed while wreaking endothelial dysfunction along its path. A non deformable embolus such as calcific atherogenic particle will travel until its girth exceeds the vessel's ability to deform.
Gas embolism is an iatrogenic event in which gas enters circulation and can result in serious morbidity and death. Animal studies have shown that rapid infusion of a large volume of air may be fatal. An arbitrary definition of microbubble size may be erroneous since only a bubble of a diameter smaller than the capillary can travel through the circulatory system without leaving an imprint and be accepted as safe. Furthermore, in biological settings, there is a dynamic, constant process of small bubble splitting into many small ones; thus, a few "harmless" microbubbles could coalesce into one injurious large bubble. The composition of a gas bubble is usually air or oxygen, although anaesthetic gas, particularly nitrous oxide, carbon dioxide and nitrogen can also result in gas emboli. It has also been found that gas composition affects bubble elimination time in the body, since each gas has its own solubility coefficient and diffusion coefficient in a given fluid. Air is inevitably introduced and the reports of gross air embolism are now uncommon because of safeguard changes in clinical practice that have ensued identification of their most frequent cause.
Extracorporeal systems have long been linked with the cause of gaseous microemboli (GME). Number of sources has been reported that GME may originate from extracorporeal circuit and oxygenator and perfusion inattention leading to the emptying of the venous reservoir and concomitantly pumping of air into patient; other causes of air introduction are through aortic root from cardioplegia delivery tubing and cannula, cardiac contractions before intracardiac de-airing is complete and also accidental reversal of flow in left ventricular venting system. The gaseous microbubbles may also be present while priming and preparing the lines for use, or newly formed as a resultant of turbulent flow in tubing and at aortic cannulation. Differences in temperature is another possible cause for bubble generation in lines since warming initiates bubble formation, such as when an active blood warming system is used. Furthermore, a gas in a bubble flowing in the bloodstream is in dynamic equilibrium with the same gas dissolved in the plasma, and a bubble will therefore grow or shrink according to the partial pressure of the gas in solution, which is largely dependent on temperature. Thus, bubbles are more likely to form and grow during rewarming phase of CPB. The course of the bubble in an extracorporeal circulation is affected by many factors, principally two opposing forces; firstly, the buoyant force of a bubble, which takes it upward and secondly, the driving force of the fluid flow, by which the bubble is carried into patients body. Also the pressure in a gas bubble tends to force the gas into solution and is inversely proportional to the radius of the bubble, therefore small bubbles are inherently unstable in blood and collapse when less than 10Âµm is diameter. Over all the clinical implications of the gaseous microemboli phenomena depends on the extent and cumulative effect of such an event.
On the other hand non deformable emboli can arise within the blood or be introduced from externally sources. Foreign particles may be present on blood contact surfaces of commercially available extracorporeal components of the CPB system. Emboli made of fragments of polyvinyl chloride tubing exposed to the roller pump and of silicone antifoam have been described extensively; however with the technological advances and current manufacturing standards have substantially reduced these hazards. A scanning electron microscopic study was carried out to quantitate the number of non-biological particles which escape capture by the arterial line filter in a standard extracorporeal circulation circuit. Five different lots of polyvinylchloride (PVC) tubing from the same manufacturer were used in closed circuit extracorporeal pump set-ups consisting of a typical length of PVC tubing, a cardiotomy reservoir, and an arterial line filter (Pall 40 microns (Âµm)). A liter of Plasmalyte was circulated through this set-up for 15 minutes at 2 liters/minute with the pump head set at almost total occlusion. The circulated Plasmalyte from each pump line was then collected and passed through a 0.22 Âµm Millipore filter. Numerous particles ranging from 5-40Âµm in diameter were observed on the surface of the filters. The study demonstrated that commonly employed tubing packs and standard roller pump designs for extracorporeal circulation are associated with continuous release of particulate matter (5-40Âµm) which is not removed by the arterial line filters most often employed. Even though with the advances of filtration methods and phenomenal change in manufacturing medical grade PVC there are still odd reports of particulate microemboli in literature. Similarly, silicone tubing's used in roller pumps are more prone to spallation due to the degree of occlusion settings and speed of rotation.
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The largest source of microemboli during open heart surgery has been reported to be the cardiotomy sucker system. It has been already known that macro and micro particles of fat are generated during CPB and are found in capillaries of kidneys, lungs, heart, brain, liver and spleen. About 70% of these fat developed during CPB enter through cardiotomy suction into the CB circuit. These emboli have typically been found to contain denatured plasma lipoproteins and lipids of varying diameter from 4 to 200Âµ in diameter. Also the fat molecules that come out of solutions consist of chylomicron aggregates or free fat containing triglycerides and cholesterol. There have also been reports of cellular debris, calcium, muscle, talc, and suture material and bone fragments being sucked by cardiotomy suction system. A study done by (Brooker et al. 1998) demonstrated the relationship between return of shed blood and brain emboli. The study reported that blood aspirated from the surgical field which was subsequently reinfused produced a greater density of small capillary and arterial dilatations then without the reinfusion of cardiotomy suction blood. This evidence is substantial in relation to instance of biological particulate being the cause of microemboli during CPB.
Other biological particulate emboli occurs due to the donor blood which has been found to contains platelets and leukocyte aggregates, bits of fibrin, red cell debris and lipid precipitates; also during the first 24 hours of storage of citrated blood at 4 Í¦ C, most of particles are platelet aggregates and particles increase with the duration of storage. The crystalloid solutions used for priming have also been found to contain inorganic debris and has the potential to be infusion into systemic circulation without proper filtration. Another report of increased elevation of serum aluminium levels postoperatively in patients who had undergone CPB was found to be linked to aluminium contamination in heat exchanger system of specific manufactures heat exchangers; however with the use of steel heat exchanger there was no elevation in plasma levels of aluminium.
A silicone, dimethyl polysiloxane, which were used as a defoaming agent in bubble oxygenators' and cardiotomy reservoirs have been described extensively as a foreign particulate material capable of infusing into systemic circulation, there has been extensive reports concerning the release of silicone into systemic circulation, also the presence of silicone in the brain and kidneys of patients who did not survive the procedure have confirmed it.
Emboli also develop from the formed blood and unformed elements of circulated blood. Biological aggregates including thrombus, platelet aggregate, and fat are also in dynamic state, with the blood allowing growth and dispersal according to prevailing conditions. Dispersal is dependent on biological chemical as well as physical mechanism and may be slower for bubbles, although experimental microvascular occlusions with platelet aggregates show reperfusion within 20 minutes. Fibrin can form within extracorporeal circulated blood if the coagulation cascade is not adequately inhibited. It has been seen when blood contacts foreign surfaces Factor XII is activated to Factor XIIa, and the coagulation cascade is initiated. Heparin in adequate doses inhibits serine esterases and blocks the coagulation at four or five different points. Most importantly heparin potentiates the action of antithrombin III and thus inhibits conversion of fibrinogen to fibrin by thrombin produced by the coagulation cascade. Fibrin tends to form in the areas of stagnant flow, on rough surfaces, and in areas of turbulence and cavitation. CPB circuits contain numerous areas of non streamlined blood flow and intraluminal projections which can develop fibrin deposits if anticoagulation is inadequate. Fibrin deposits are prone to develop at the connections, within oxygenator, and in arterial line filters.
Plasma proteins are denatured during contact with CPB synthetic surfaces and during passage through oxygenators. Denaturation of plasma proteins alters immunological milieu and complement system and further affects adhesion of platelets to synthetic surfaces. Fat emboli also develop from blood passed through CPB systems. These emboli are formed due to due to the denaturation of plasma lipoproteins and lipids that cause fat to come out of solution. These emboli are aggregates of chylomicrons and contain principally triglycerides and cholesterol. They are of varying sizes and stain with oil red O or osmium tetroxide stains during histological studies of tissues.
Furthermore, contact between blood and synthetic surfaces activates platelets and causes the formation of platelet aggregates. Most platelets aggregates probably disaggregate in microcirculation; however some platelets aggregate emboli have been observed in central nervous system of patient who died after open heart operations. Also leukocyte aggregates have also been reported to occur during CPB applications, these aggregates release lysosomal enzymes which in turn cause extravasation of plasma into surrounding tissues. CPB has also been shown to reduce the ability of red cell deformation during passage through the microcirculation.
Mechanism of tissue damage
One of the first immediate and most rapid event following emboli in circulation is the obstruction of blood flow in the capillary distal and proximal to the occluding particle. Due to the blockade ischemia occurs with the changes of pressures in the circulation and interstitium around the blood vessel. Instantaneously, the inflammatory process is initiated with complement response. Neutrophils play a central role in mediating air emboli induced lung injury. They aggregate around emboli to produce clumps. A local destructive process takes place by superoxide and hydroxyl radical production and proteolytic enzyme release. These molecules have been reported to increase membrane permeability to fluids and proteins and facilitate pulmonary oedema. Further study reported that leukopenia occurs which attenuates the increase in microvascular permeability particularly in case of microgaseous emboli. Also this pathophysiologic process is found to be independent of composition of microemboli and starts as the circulating microemboli is trapped in a small arteriole or in a capillary.
Mechanical damage occurs as the emboli travel in the blood stream until it is lodged in the microcirculation. Along the way emboli are compressed against the endothelial capillary wall, causing functional stripping of endothelial cells and increase of large -pore radii. In addition, gaps between endothelial cells are created; normally endothelial cells are tightly joined to prevent shift between intravascular fluid and surrounding tissues. This functional stripping and gap formation allows transfer to fluid between these compartments causing interstitial oedema. The hydrostatic pressure upstream to the emboli increases causing further interstitial oedema. Downstream to the obstruction, tissue ischemia depending is sensitivity to hypoxic conditions.
Activation of complement by circulating microemboli commences at the emboli interface with blood and formed an element that surrounds it. There are reports that prior depletion of complement proteins before the initiation of bypass resulted in lowered incidences of microemboli related phenomena in some invivo studies, also increased level of activated plasma proteins C3a and C5a, correlated with the occurrences. Since C3a and C5a trigger polymorphonuclear leukocytes (PMNs) and stimulate mast cells to release histamine, which increases vascular permeability. Activated PMNs further augment tissue damage by releasing cytotoxic substances such as active oxygen metabolites and arachidonic acid products; these metabolites further cause liquid peroxidation to endothelial cell membranes. The arachidonic acid products such as prostaglandins and leukotrienes are vasoactive factors, and all alter microvascular permeability.
Clotting system is also affected by microemboli in two ways, firstly by activating coagulation and by inducing platelet aggregation resulting in clot formation at the emboli proximity. Further fibrinolysis and local reaction to thrombus occurs. The emboli surface acts as a foreign substance and activates the coagulation system. As is case of gaseous microemboli the gas-blood interface adsorbs macromolecules that are normally present in blood. This adsorption provokes molecular conformational changes, such as unfolding and exposing regions of proteins that trigger blood coagulation. Studies have further shown that platelets adhere to the gaseous microemboli surfaces, where they act as platelet agonists with respect to aggregation. Additionally, these gaseous microemboli induced endothelial damage causes tissue factor expression and subsequent platelet activation resulting in thrombus generation.
Microemboli may originate from various sources throughout the cardiopulmonary circuit. Oxygenator, the fundamental part of the CPB circuit is one of the causes of emboli creation, its fundamental requirement is the provision of adequate gas exchange without the damage to formed blood elements and without the introduction into systemic arterial circulation of gaseous and particulate microemboli. It has been described in the literature that bubble oxygenators used earlier released (a) gaseous microemboli (b) damage to formed blood elements (c) inability to maintain optimal physiological levels of PaO2 and PaCO2 during cardiopulmonary bypass. Bubble oxygenators were prone to gaseous microemboli creation due to the direct gas and blood Interface, bubbles with the diameter greater than 35 to 40Âµm have been reportedly associated with CPB morbidity and mortality, unlike those with smaller diameters. With the design change and the use of better chemical defoaming agents the generation of GME has been considerable reduced the number and sizes of gaseous microemboli produced by bubble oxygenators. Finally wide spread use of membrane oxygenators have also eliminated the source of microemboli arising from antifoam agents.
On the other hand membrane oxygenators do not have tendency to generate GME due to presence of interface between gas and blood phase. A study conducted on membrane and bubble oxygenator demonstrated a significant reduction in GME production in membrane oxygenator. However particles generated in vivo by oxygenators during CB with heparinized blood have been described in variety of studies. Reports of particles found in oxygenators after priming fluid before connection of the circuit to the patient have also been documented. Studies have also reported that linen fibres, originating from cloth used to wrap parts of oxygenator before sterilization have were found in primed and rinsed CB circuits.
The physical damage to membrane material has been reported to allow release of GME into the blood, or elevated transmembrane pressure rations causes bubble formation on the blood side of the membrane. As evident one of the most important items of the extracorporeal circuit is oxygenator. With special filter and defoamer materials, emboli can be captures in the oxygenator. The fiber configuration of the oxygenator will affect the capability of air handling and pressure drop in the membrane compartment. Better capability of air handling and less pressure drop will reduce emboli amount and alleviate the stress injury of blood cells. A study which compared the capability of air handling and pressure drop between pre-oxygenator and post oxygenator between three oxygenators in a stimulated adult model of CPB. The results indicate that oxygenator design has a considerable effect on the air handling capability and pressure drop pre and post oxygenator.
There is increasing evidence that platelet-protein interaction with oxygenator surface is responsible for many of the undesirable hemostatic consequences of CPB. Blood flow through the oxygenator for gas exchange predisposes blood and formed elements to foreign surfaces, this process alters normal hemostatic balance, immunological and complement proteins are also altered. Platelets are also activated which leads to formation of platelet aggregation and consequently thrombocytopenia occur. This activation of blood and formed elements with protein adsorption are some of the causes of emboli formation in CB oxygenators. In order to overcome blood activation various biocompatible strategies have been employed. The first biocompatible treatments were based on heparin bonding, either ionic or covalent. Heparin is an anticoagulant; it binds to the enzyme inhibitor antithrombin III (AT) causing a conformational change that result in its activation through an increase in the flexibility of its reactive site loop. The activated AT then inactivates thrombin and other proteases involved in blood clotting, most notably factor Xa. Subsequently, many different kinds of biocompatible treatments became available for clinical use. Even taking into account that some biological differences exist among the different biocompatible treatments, the general philosophy is to mimic the endothelial surface by coating the CPB circuit and oxygenators. Studies exploring biochemical markers of inflammation, activation of hemostatic system, and platelet aggregation have demonstrated a beneficial effect of these biocompatible treatments in terms of decrease of the systemic inflammatory reaction to CPB, a lower degree of hemostatic system activation, a prevention of platelet adhesion and aggregation.
Pumps and CPB tubing
Silicone tubing present in roller pumps has been associated with spallation during the course of cardiopulmonary bypass. This was further confirmed with histological studies which found the presence of silicone particles in liver, spleen, and other organs. A study which compared silicone tubing to polyvinyl chloride tubing in roller pump heads showed that roller pump produce spallation and sequestration of particles ranging up to 25Âµm in diameter. Clearly, this indicates that spallation of silicone tubing in roller pumps is one of the causes of emboli creation during CPB application. Furthermore, the study also reported that with the increase in flow rate and increase in occlusion pressures the rate of spallation was two folds. It has also been reported that these particles once introduced in systemic circulation initiate inflammatory response and fibrosis of organs such as liver.
Centrifugal pumps on the other hand have different working principle, they consist of vaned impeller inside of smooth plastic cone which with rotation, propel blood by centrifugal force. Since there is no contact compression of tubing for pressure generation they theoretically avoid spallation problems, however they are after load dependent and with negative inflow pressure they are most likely to de-prime if 30 to 50ml of air enters blood chamber. Centrifugal pumps have been reported to generate 900mmhg of forward pressure and 400 -500mmhg of negative pressure which is the reason for less cavitation and considerably reduced gaseous microemboli generation as compared to roller pump. Quantitative bench study to investigate differences in microbubble generation reported that with similar blood flow, constant head pressure, and maintaining the temperature of blood at 25 Í¦ and 36 Í¦ C; microbubble creation by a roller pump was significantly more than centrifugal pump (Tayama et al. 1999). Particulate emboli formation has also been associated with centrifugal pumps, it is been reported that friction between blood and impeller bearings causes microparticle creation in centrifugal pumps; although to a much lesser degree as compared to roller pumps.
On the other hand medical-grade polyvinyl chloride tubing the main component of CPB circuits is mainly used due its desirable characteristics including transparency, resilience and kink resistance. It also has low spallation rate, inertness, smooth non-wettable inner surface and toleration for heat sterilization. Silicone and rubber tubing used in past had high hemolysis and spallation rates and there use was discontinued. On its own un-plasticized PVC tubing is a rigid material and needs to have liquid property added for flexibility, a critical requirement in perfusion tubing. The most widely used plasticizer is di-(2-ethylhexyl) phthalate (DEHP), which is in-cooperated into PVC at a level between 30 and 40% in order to achieve the required flexibility. However DEHP plasticizer providing the flexibility tends to migrate to the surface of the material and mix with blood. Studies have shown that the surface which blood encounters during cardiopulmonary bypass is not PVC, but largely DEHP that has migrated to the surface. On the other hand it has been establish that blood response to plasticized PVC is influenced not only by the Poly (vinyl chloride) itself, but also by the nature of plasticizers employed and the concentration of plasticizers in the PVC formation. Also due to the manufacturing defects plastic particles and uneven surfaces have also been reported cause of microemboli source with respect to CPB use. A study by (Knopp et al. 1982) reported the presence of particles in isolated cardiopulmonary tubing, they found that tubing was associated with continuous release of particulate matter (5-40Âµm) and were not subsequently removed by arterial filters mostly employed in circuits.
PVC tubing is one of the largest surfaces that interact with blood and formed elements. Due to its non endothelial origin activation of blood has been reported at a great deal in the literature which has also been linked to platelet aggregation and emboli formation. A study by (Gu et al. 1998) showed that biocompatible treatment with surface modifying agents (SMA) improved blood compatibility. Assessment with labeled monoclonal antibody against platelet glycoprotein IIIa they were able to show significant decrease in platelet deposition on CB circuit as compared to circuit with no coating. They also reported that patterns of platelet activation was modified by SMA treatment and was further confirmed by a less pronounced release of ß-thromboglobin. Moreover, reduced generation of F1+2 fragments also indicated decreased activation of prothrombin involved in coagulation process(Gu et al. 1998).
Reservoir is another integral part of CPB; they may be hard shell or soft shell. In adult cardiac surgery hard-shell reservoir is mostly used, however collapsible ones are also used depending on institutional guidelines. Hard shell reservoirs comprise on average of polyester depth filter, polycarbonate housing and a polyurethane defoamer. Over all reservoirs provides capacitance, a high- efficiency filtration, defoaming and the removal of foreign particles. Fluid level in the reservoir is maintained throughout the duration of CPB, it also act as a safety mechanism which reduces the risk of perfusion accidents, such as pumping of air into the arterial cannulation when venous return to reservoir is occluded. In addition scavenged blood form the operating field is returned to cardiotomy reservoir via suckers. Studies have reported that oxygenators alter the blood in a manner that is detrimental to the tissues being perfused and these effects are exaggerated after blood has been aspirated from heart with resultant red cell destruction and formation of gaseous and particulate emboli. Furthermore, scavenged blood is a potent source of both particulate and gaseous microemboli. Cardiotomy suction blood has also been reported to have high level of cellular aggregation and trauma which is regarded as one of the biggest sources of microemboli.
Literature reports presences of solid particles as result of manufacturing process have been isolated in venous reservoirs and cardiotomy reservoirs. Also fibres, plastic particles, antifoam sponges and excess moulding material have also been found during filtration process. Research has also provided evidence that particulate emboli has been a serious threat to patients undergoing cardiopulmonary bypass, reports of instances where particulate matter was present after priming of circuits are numerous, however the exact composition has been unknown. With the use of scanning microscope and x-ray diffraction prebypass filters and cardiotomy reservoirs were studied and tested for particulate contaminants, a total of 341.5 particles were identified with majority of particles between 2 and 5Âµm in diameter (Merkle, Böttcher & Hetzer 2003). This clearly indicates venous reservoirs and cardiotomy suckers as sources of particulate emboli during CPB use.
(Lynch & Riley 2008) reported a case of microemboli generation by a loose cap on a connector. An extracorporeal circuit was fully primed and ready to be used, ultrasonic detector showed large number of embolic signals. Pump was fully checked again and the source of air was eventually traced to a loose cap on a side port of the venous reservoir. Once the cap was tightened, the embolic load and counts quickly decreased. Furthermore, they also traced the source of air to partly primed prebypass filter. This clearly indicated the possibility of air entry through loose connectors, connections, and tears and breaks in CPB circuitry. Several other studies have also demonstrated the occurrence of cerebral emboli in association to specific perfusionist events, like blood sampling, drug injection, and addition of blood to cardiotomy circuit. (Taylor et al. 1999) reported that perfusion interventions account for large number of emboli creation during conduct of cardiopulmonary bypass, they demonstrated in their study a relationship between interventions of blood sampling and infusion of drugs to CPB circuit. In their study mean embolic rate was calculated during blood sampling and drug administration into the venous reservoir, their findings suggested that majority of microemboli that occur during CPB consisted of gaseous microemboli. Small gaseous microemboli contained within the syringe used for blood sampling were demonstrated to enter the venous reservoir and found their way into oxygenator, this practice of inadequate de-airing and not discarding of stagnant blood were consistent with embolic load apparent on ultrasonic detector. However, when proper de-airing of syringes and disposal of stagnant blood was done the embolic load was significantly reduced.
On the other hand they were also able to demonstrate that these gaseous emboli were able to traverse the arterial filter which was 35Âµm filter, clearly indicating the inability of filter to gaseous micro emboli. The method by which gaseous air traverses arterial filter was not entirely clear; however gas bubble dynamics and its ability of distortion into a sausage shape might have been a possible explanation.
CPB circuit is complex and it is a composition of many connectors and tubing for versatility and ease of use. On one hand connectors provide easy way to reassemble or modify the circuit according to the need but on the other hand connectors cause break in the smoothness or tubing and place for turbulence and blood stasis. Turbulent flow has been linked to increased stress to blood and formed elements, (Kameneva et al. 2004) demonstrated in a comparative study the effects of laminar and turbulent flows on blood hemolysis. The study was done with a suspension of bovine blood driven through a closed circulating loop by a centrifugal pump. Viscosity of blood was changed with addition of saline and dextran respectively in-order to produce laminar and turbulent flow and maintaining the shear stress. Reynolds numbers ranging from 300-5,000 were generated and subsequently hemolysis rates were measured. Over all by keeping the shear stress constant, it was apparent that rates of haemolysis was significantly higher in turbulent flow as comparative to laminar flow. This study provides evidence about the possibility of emboli formation within the CPB circuit and thereby increases the morbidity and mortality in cardiac surgery due to CBPB use.
Priming solutions and additives to CB circuit have been associated with introduction of gaseous and particulate emboli.
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