Microembolism during cardiopulmonary bypass: a comparison of bubble oxygenator with arterial line filter and membrane oxygenator alone

Perfusion ◽  
1991 ◽  
Vol 6 (2) ◽  
pp. 99-103 ◽  
Author(s):  
Steven Griffin ◽  
Wilfred Pugsley ◽  
Tom Treasure
Blood ◽  
1987 ◽  
Vol 69 (1) ◽  
pp. 324-330 ◽  
Author(s):  
YT Wachtfogel ◽  
U Kucich ◽  
J Greenplate ◽  
P Gluszko ◽  
W Abrams ◽  
...  

Abstract Cardiopulmonary bypass, especially when prolonged, may result in hemostatic failure and pulmonary dysfunction, which has been attributed to changes in platelets and leukocytes, respectively. It has been well documented that contact of blood with synthetic surfaces causes platelet activation. In this report, we explore mechanisms of the activation of neutrophils during simulated in vitro extracorporeal circulation and document the release of neutrophil lactoferrin and elastase during clinical cardiopulmonary bypass (CCB). Inhibition in the simulated circuit by prostaglandin E1 (PGE1) and lidocaine suggests different mechanisms for release of neutrophil-specific proteins. During CCB with a bubble oxygenator it was observed that platelet counts fell to 42% +/- 2% of baseline. In addition, beta- thromboglobulin antigen (beta TG), a platelet-specific, alpha-granule protein marker reflecting the release reaction, increased from 0.15 +/- 0.05 to 0.84 +/- 0.11 microgram/mL. Neutrophil counts decreased to 67% +/- 7% of prebypass levels but then gradually rose as bypass continued. Both lactoferrin, a neutrophil-specific granule marker, and neutrophil elastase, an azurophilic granule marker, increased in plasma threefold to 1.66 +/- 0.33 micrograms/mL and 1.65 +/- 0.68 microgram/mL, respectively, just before bypass was stopped. When fresh heparinized human blood was recirculated within an extracorporeal membrane oxygenator bypass circuit for 120 minutes, plasma beta-TG rose to 5.13 micrograms/mL, lactoferrin increased from 0.13 +/- 0.04 to 1.62 +/- 0.22 micrograms/mL, and neutrophil elastase rose from 0.05 +/- 0.02 to 1.86 +/- 0.41 micrograms/mL. At 120 minutes, lidocaine (100 mumol/L), which inhibits neutrophil activation, delayed release of lactoferrin (1.33 +/- 0.26 micrograms/mL) and markedly inhibited release of elastase (0.24 +/- 0.05 microgram/mL) but did not inhibit release of beta-TG antigen (5.66 micrograms/mL at 120 minutes). PGE1 (0.3 mumol/L) inhibited significantly the release of beta-TG (0.31 microgram/mL) and elastase (0.52 +/- 0.11 microgram/mL) and attenuated the release of lactoferrin (1.57 +/- 0.45 micrograms/mL).


Perfusion ◽  
1987 ◽  
Vol 2 (4) ◽  
pp. 289-295 ◽  
Author(s):  
Ludwig von Segesser

Ten mongrel dogs were connected to cardiopulmonary bypass by cavoaortic cannulation, classic roller pump and either Bentley BOS-CM 40 hollow fibre membrane oxygenator or Polystan VT5000 Venotherm bubble oxygenator for eight hours, with mean flow rate of 100 ml/kg min. Platelet counts (all values corrected by prebypass haematocrit) were significantly lower in the bubble oxygenator group after two hours of cardiopulmonary bypass (p < 0·01). Plasma haemoglobin production was significantly higher after two hours of cardiopulmonary bypass in the bubble oxygenator group (p < 0·01). Venous oxygen saturation (SvO2) was above 65% during the eight hours perfusion in the membrane oxygenator group. In the bubble oxygenator group, however, SvO2 was below 60% after six hours of cardiopulmonary bypass. After eight hours perfusion the difference in SvO2 between the two groups was significant (p < 0·05). Thus membrane oxygenators such as the Bentley BOS-CM 40 appear to be indicated in cardiopulmonary bypass of more than two hours duration.


Perfusion ◽  
1987 ◽  
Vol 2 (1) ◽  
pp. 27-33 ◽  
Author(s):  
PW Boonstra ◽  
Fee Vermeulen ◽  
JA Leusink ◽  
EH de Nooy ◽  
A. van Zalk ◽  
...  

We determined to what extent a 27 micron depth filter (Bentley Polyfilter bypass blood filter PF427, Bentley Lab., Irvine, California, USA) in the arterial line of a bubble oxygenator (BO) system is responsible for the difference in haemocompatibility between this BO system and a membrane oxygenator (MO) system in which no arterial line filter is used. We studied three groups of patients subjected to long perfusions of approximately three hours: BO perfusion with ( n = 8) and without ( n = 8) the arterial line filter and MO perfusion ( n = 10) without filter. Platelet and erythrocyte damage were evaluated at seven sampling points during perfusion. Also pre- and postoperative bleeding times and postoperative blood loss and blood transfusions up to 18 hours after perfusion were determined. We found that the 27 micron depth filter in the arterial line impairs the haemocompatibility of the BO only to a small extent; the MO remains haematologically superior over the BO even when the arterial line filter is absent from the BO circuit.


2005 ◽  
Vol 33 (3) ◽  
pp. 295-300
Author(s):  
S Hamanaka ◽  
K Tanemoto ◽  
E Inagaki ◽  
T Yamasawa ◽  
K Yoshida ◽  
...  

We developed a system to measure nitric oxide (NO) concentration during cardiopulmonary bypass in anaesthetized pigs (n = 6). A T-shaped connector, attached to an NO sensor, was mounted in the extra-corporeal circuit at two measuring sites: proximal to the membrane oxygenator (venous side) and distal to the arterial line filter (arterial side). After performing a preliminary validation study, we measured plasma NO concentration before and during total cardiopulmonary bypass circulation (non-pulsatile flow 1.5 l/min) and without pulmonary ventilation. After establishing bypass, PaO2 was 318-393 mmHg; when PaO2 was decreased to 80-100 mmHg, plasma NO concentration in the arterial circuit fell by 39.2 ± 15.6 nM. There was no observable change in plasma NO concentration at the venous circuit. This new system could be useful in monitoring NO concentration during cardiac surgery with cardiopulmonary bypass, and for understanding the possible pathophysiological roles of hyper-nitric oxaemia in cardiopulmonary bypass-related cardiovascular complications.


Blood ◽  
1987 ◽  
Vol 69 (1) ◽  
pp. 324-330 ◽  
Author(s):  
YT Wachtfogel ◽  
U Kucich ◽  
J Greenplate ◽  
P Gluszko ◽  
W Abrams ◽  
...  

Cardiopulmonary bypass, especially when prolonged, may result in hemostatic failure and pulmonary dysfunction, which has been attributed to changes in platelets and leukocytes, respectively. It has been well documented that contact of blood with synthetic surfaces causes platelet activation. In this report, we explore mechanisms of the activation of neutrophils during simulated in vitro extracorporeal circulation and document the release of neutrophil lactoferrin and elastase during clinical cardiopulmonary bypass (CCB). Inhibition in the simulated circuit by prostaglandin E1 (PGE1) and lidocaine suggests different mechanisms for release of neutrophil-specific proteins. During CCB with a bubble oxygenator it was observed that platelet counts fell to 42% +/- 2% of baseline. In addition, beta- thromboglobulin antigen (beta TG), a platelet-specific, alpha-granule protein marker reflecting the release reaction, increased from 0.15 +/- 0.05 to 0.84 +/- 0.11 microgram/mL. Neutrophil counts decreased to 67% +/- 7% of prebypass levels but then gradually rose as bypass continued. Both lactoferrin, a neutrophil-specific granule marker, and neutrophil elastase, an azurophilic granule marker, increased in plasma threefold to 1.66 +/- 0.33 micrograms/mL and 1.65 +/- 0.68 microgram/mL, respectively, just before bypass was stopped. When fresh heparinized human blood was recirculated within an extracorporeal membrane oxygenator bypass circuit for 120 minutes, plasma beta-TG rose to 5.13 micrograms/mL, lactoferrin increased from 0.13 +/- 0.04 to 1.62 +/- 0.22 micrograms/mL, and neutrophil elastase rose from 0.05 +/- 0.02 to 1.86 +/- 0.41 micrograms/mL. At 120 minutes, lidocaine (100 mumol/L), which inhibits neutrophil activation, delayed release of lactoferrin (1.33 +/- 0.26 micrograms/mL) and markedly inhibited release of elastase (0.24 +/- 0.05 microgram/mL) but did not inhibit release of beta-TG antigen (5.66 micrograms/mL at 120 minutes). PGE1 (0.3 mumol/L) inhibited significantly the release of beta-TG (0.31 microgram/mL) and elastase (0.52 +/- 0.11 microgram/mL) and attenuated the release of lactoferrin (1.57 +/- 0.45 micrograms/mL).


1994 ◽  
Vol 17 (10) ◽  
pp. 543-548 ◽  
Author(s):  
Y.J. Gu ◽  
P.W. Boonstra ◽  
C. Akkerman ◽  
H. Mungroop ◽  
I. Tigchelaar ◽  
...  

The contact of blood with the artificial extracorporeal circuit causes a systemic inflammatory response due to blood activation. In this study, we compared two different paediatric membrane oxygenators used for extracorporeal circulation: a hollow fibre membrane oxygenator (Dideco Masterflo D-701, n=10), and a flat sheet silicone membrane oxygenator (Avecor Kolobow 800-2A, n=10). Blood compatibility was indicated by measuring complement activation as well as leukocyte and platelet activation. In patients perfused with a flat sheet membrane oxygenator, concentrations of complement split products C3a were significantly increased 30 minutes after the start of bypass (p<0.01), whereas only a mild increase of C3a was found in patients perfused with a hollow fibre membrane oxygenator. Leukocyte and platelet counts dropped uniformly in both groups after the start of bypass mainly due to hemodilution. Activation of leukocytes and platelets identified by both plasma β-glucuronidase and β-thromboglobulin was similar in both groups. Infants perfused with a flat sheet membrane oxygenator received significantly more donor blood than those perfused with a hollow fibre oxygenator (p<0.05). These results indicate that when used during paediatric cardiopulmonary bypass, a flat sheet membrane oxygenator has a higher complement activity than a hollow fibre membrane oxygenator, which is probably due to the relatively larger blood-surface contacting area of the oxygenator.


1991 ◽  
Vol 51 (4) ◽  
pp. 573-578 ◽  
Author(s):  
Y.J. Gu ◽  
Y.S. Wang ◽  
B.Y. Chiang ◽  
X.D. Gao ◽  
C.X. Ye ◽  
...  

1985 ◽  
Vol 16 (5) ◽  
pp. 490-499
Author(s):  
Tadanori KAWADA ◽  
Hiroaki OSADA ◽  
Shigeki FUNAKI ◽  
Kazumi ARASE ◽  
Masayuki HOSON ◽  
...  

Perfusion ◽  
1993 ◽  
Vol 8 (4) ◽  
pp. 337-344 ◽  
Author(s):  
Juha Aittomäki

The correlation between pCO2 values in blood and in exhaust gas from the oxygenators was examined during cardiopulmonary bypass (CPB) using one bubble oxygenator and three membrane oxygenators. Forty-seven CPBs were performed, 17 with Compactflow® (Dideco, ltaly), 10 with Maxima® (Medtronic Inc., USA), 10 with Cobe CML®(Cobe Laboratories, USA) membrane oxygenators and 10 with Hi-Flex® (Dideco, Italy) bubble oxygenators. Blood samples were taken both from arterial and venous lines of the oxygenator. A capnometer was connected to the oxygenator gas exhaust port and CO2 fraction was measured at the time of drawing blood samples. CO2 pressure in the gas phase was calculated from the product of the CO2 fraction and water vapour- corrected barometric pressure. Blood gases were measured at 37°C and the pCO2 value was corrected to the temperature of the arterial line. The correlation between blood and exhaust gas pCO2 was good in all the oxygenators examined, ranging from 0.921 to 0.976. The standard error of estimate (SEE) was in the range of about ± 2 mmHg for all the oxygenators. The systematic error (slope and intercept of the correlation line) varied depending on the construction of the oxygenator, with countercurrent design having the best overall correspondence. Based on the results of this study it can be concluded that arterial or venous CO 2 pressure can be monitored with a capnometry device coupled to the oxygenator gas outlet port. The use of a 'target FCO2 line' or a calculator program is proposed in order to aid the perfusionist in adjusting the oxygenator gas flow to attain normocarbia during CPB.


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