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Serdar Gunaydin, MD 

Clinical Professor of Cardiovascular Surgery 

University of K.Kale- Turkey 

Kevin McCusker, CCP, PhD 

Assistant Professor of Cardiovascular Surgery 

New York Medical College, NY

Air handling: Revisit 

Definitions, , types and tissue effects of macroeboli and 

microemboli 

Localization, sources and prevention of air in cardiac surgery 

Detection & Quantification of Air Particles 

Evidence based scientific research on air handling 

Our studies 

‣Air handling & Cardiac surgery. AmSECT Td Today, Nov, 2008 

‣Clinical 

Evaluation Of Minimized Extracorporeal Circulation 

in High 

Risk 

Coronary Revascularizat 

zation. Perfusion 2009 

‣The 

Impact of the Intensity of Microemboli on Postoperative Neurocognitive 

Outcome in Coronary Revascularization 

Novel 

approcah to air handling in cardiac surgery

Although modern techniques of Whereas the incidence of adverse 

cardiopulmonary bypass and 

better circuit designs have 

patient outcome attributable to 

gross air embolism was once 

minimized the fatal cases of 

every 2500 cases in the 1970s, the 

massive air embolism, recent 

incidence in the 1990s has fallen to 

investigations suggest that 

once every 30 000 cases according 

systemic air microembolization 

to the most recent national survey 

derived from extracorporeal 

Previous studies have reported 

sources still represents a 

that between 6% and 9% of the 

common problem during 

total number of emboli detected 

conventional CPB 

during CABG occur during the 

High numbers of air 

onset of CPB 

microemboli are one factor 

 

These embolic signals are assumed 

contributing to a reported 50- 

to represent air bubbles delivered 

70% rate of cognitive deficits 

into the systemic circulation as a 

one week after CABG and 30% 

result of air retained in the 

rate of long-term 

components of the extracorporeal 

neuropsychologic impairment 

circuit

Recent design improvements and current 

strategies t of CPB in some instances have not been 

proven to reduce 

•Vacuum-assisted 

and may, in 

venous 

fact, increase the 

risk of gross drainage 

air embolism during CPB 

• Drug injection •Low-prime perfusion circuits 

•Aortic cannula •Carbon type dioxide and placement flooding of 

•Internal properties the operative of oxygenator field 

and filters 

•Levels of vacuum (

Cardiovascular function is affected by the compressible air causing obstruction to 

right ventricular ejection at the level of the pulmonary outflow tract 

Slower infusions of air become trapped at the level of the pulmonary arterioles 

causing pulmonary arterial hypertension and subsequent right ventricular failure 

The effect of microbubbles entering the pulmonary arterioles gradually is not only to 

obstruct flow but, in addition, neutrophils are attracted to the network of fibrin, red 

blood cells, fat globules and platelets that build up around the bubble 

The ultrastructural damage that results from this leads to increased basement 

membrane permeability and, ultimately, to pulmonary edema 

Sufficient pressure builds up on the right side of the heart to push gas through the 

pulmonary circulation to the left atrium. Any increase in pulmonary artery pressure 

will favour the transfer of air into arterial circulation



microemboli 




Our studies 


‣Clinical 


in High 

Risk 



‣The 



Novel 


We can divide emboli into macro and micro categories according to size, 

the former occluding flow in arteries 200 μm or greater in diameter and 

the latter, in smaller arteries, arterioles, and capillaries 

Distinction on the basis of size is no guide to the composition of emboli 

Such a distinction may reflect different clinical manifestations: 

• A single macroembolus might result in hemiplegia, but a solitary microembolus is 

unlikely to have a noticeable effect except in very susceptible tissue such as the 

retina 

•Clinical effects of microemboli should arise only when these emboli are numerous 

and can be expected to present a diffuse pattern of CNS injury rather than a focal 

deficit

GAS BUBBLES 

BIOLOGIC AGGREGATES 

Gaseous emboli consist INORGANIC of air or 

DEBRIS 

Emboli of biologic aggregates including 

anesthetic gas, particularly Embolizationb nitrous oxide of fragments of polyvinyl thrombus, l chloride 

platelet aggregates, and fat are 

The gas in a bubble tubing flowing exposed in the to the roller pump 

also 

and 

in 

of 

a 

silicone 

dynamic state, with the blood 

bloodstream is in dynamic antifoam equilibrium have been described,but 

allowing 

current 

growth or dispersal according to 

with the same gas dissolved manufacturing the standards have substantially 

prevailing conditions 

plasma, and a bubble reduced will therefore these hazards grow 

Dispersal is dependent on biochemical as 

or shrink according to Many the partial studies pressure of experimental microembolism 

well as physical mechanisms and 

of the gas in solution, have which used is largely glass and latex microspheres 

may 

of 

be 

known 

slower than for bubbles, although 

dependent on temperature size, and the tissue effects of these 

experimental 

artificial 

microvascular occlusions with 

platelet aggregates showed reperfusion 

Bubbles are more likely microemboli to form and are consequently well 

within 20 minutes 

grow during the rewarming documented 

phase of CPB 

Solid emboli can migrate a short 

Platelets 

distance 

contain vasoactive substances and 

Because the pressure in a bubble tends 

downstream after initial impact and 

can 

occlusion 

also cause 

of 

endothelial 

a 

injury 

to force the gas into solution and is 

vessel but cannot disperse 

Thrombi can arise from within the heart, 

inversely proportional to the radius, 

most commonly from the left atrial 

small bubbles are inherently unstable in 

appendage or a left ventricular aneurysm, or 

blood when less than 10 μm in diameter 

from the CPB circuit if heparinization is 

Similar considerations apply when a 

Inadequate heparin may contribute to fat 

bubble embolus occludes a blood vessel; 

embolism by stimulating endothelial 

dispersal seems to occur rapidly, 

lipoprotein p lipase, and denaturation of 

although endothelial injury and endorgan 

damage may persist 

plasma lipids, but the principal source of 

proteins during CPB may also precipitate 

cholesterol embolism is probably from largevessel 

atherosclerotic plaques



microemboli 




Our studies 


‣Clinical 


in High 

Risk 



‣The 



Novel 


Major Significance 

 

 

 

 

 

 

 

Atrial fibrillation 

Valvular (mitral) 

stenosis 

Myocardial infarction 

Thrombus in left 

ventricle 

Infective endocarditis 

Myxoma in the left 

atrium 

Dilated 

cardiomyopathy 

Minor Significance 

 

 

 

 

 

Mitral valve prolapse 

Patent foramen ovale 

Aneurysm of atrial 

septum 

Valvular (aortic 

aortic, mitral) 

calcifications 

Prosthetic heart valve

Atherosclerotic artery Cardiopulmonary 

disease 

bypass 

Carotid stenosis 

 

Carotid 

Intracranial artery 

endarterectomy 

stenosis 

 

Angiography 

Aortic arch plaques 

 

Percutaneous 

Dissection of carotid 

transluminal 

arteries 

angioplasty 

Aortic aneurysm

Careful dearinig of intravenous catheters and CPB circuit 

Incorporation p of air detector and bubble traps in intravenous 

catheters and in the CPB circuit 

Incorporation of arterial catheter filter 

Constant attention to the oxygenator blood level 

Incorporation of blood level sensor/shut off in the oxygenator design 

Testing of vents and suckers in saline before CPB 

Check of integrity and direction of perfusion catheters 

Immediate cessation of pump and inspection on any abnormal noise 

Avoidance of traffic around the perfusion catheters 

Secure fixation of the oxygenator 

Adequate vent on the oxygenator to avoid pressurization



microemboli 




Our studies 


‣Clinical 


in High 

Risk 



‣The 



Novel 


IN VIVO 

IN VITRO 

IN VITRO 

Ultrasound 

Histopathology 

On-line IN VIVO 

Blood 

detection 

Sampling 

of echogenic In early material studies, in Hill the examined tubing of the extracorporeal brains circuit was first 

reported Retinal by Studies and Austen Other by and Swank End-Organ Howry of 133 in the patients Studies in1950s 1965 

who on the died filtration after an of 

open 

Doppler The retina stored ultrasound provides blood has 

in an heart relation excellent operation. to opportunity blood Fat transfusion embolism to study led was the to 

the cerebrovascular 

also microcirculation been the used development to detect in vivo 

emboli most of the common in screen the carotid finding filtration arteries and method 

occurred and the in 

middle cerebral arteries 

Continuous It also for provides the standing-wave detection ideal nearly of model microaggregates (non-Doppler) all patients for the study ultrasound in of blood 

embolic has events a very because high detection of the absence rate for solid 

microparticles 

of arteriolar 

 

The pressure collaterals required More and the to recent clear force demarcation studies blood at have a given of identified ischemic areas 

Although Quantification flow it is rate technically of through the platelet-fibrin 

extent possible a screen of retinal filter for microaggregates ultrasonic ischemia of given methods pore was achieved size 

in canine 

to differentiate by digital image between analysis gaseous and 

solid of the emboli ischemic was by measured 

spectral areas 

retinal vessels after CPB, and these 

analysis, this It should has not be been microaggregates noted feasible that both as an microaggregates on-line have been technique 

associated with 

and 

More importantly, gaseous microbubbles calibration microfocal are ultrasound ischemic neuronal 

inherently for unstable 

quantitative injury. Use 

studies presents serious 

difficulties, entities particularly of a specialized histochemical technique 

in thein blood blood 

and can be altered by foreign 

Conversion has revealed cerebral arteriolar and 

surfaces; of detected hence, signals any manipulation 

into ``counts'' of blood 

depends on software programming variables, and 

it is unclear 

capillary lesions after CPB 

samples for measurement has Ma high probability 

whether an Careful histopathology still provides 

of increase altering such in signal emboli 

amplitude reflects an increase in the number or the size of emboli 

evidence of embolic problems in the CNS 

after cardiac surgical interventions

Online devices employ ultrasound 

technology to detect individual gaseous 

microemboli in blood flowing through an 

extracorporeal circuit 

The unit has demonstrated count rates 

exceeding 1000 emboli per second, with 

diameters from 10 microns to the connector 

diameter, and with flow rates between 2.0 

L/minute and 6.0 L/minute 

Up to three sensors may be placed 

• venous inlet 

• in between bubble trap and oxygenator 

• on arterial line after arterial filter

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microemboli 




Our studies 


‣Clinical 


in High 

Risk 



‣The 



Novel 


Diameter of 

Volume of 

No. of 

Each Bubble Each Bubble Bubbles 

Total Volume 

Surface Area 

of Each 

Bubble 

Total Surface 

Area 

1 cm = 10 mm 05mL 0.5 1 05mL 0.5 314cm 3.14 2 314cm 3.14 2 

0.1 cm = 1 mm 0.5 µL 1,000 0.5 mL 3.14 mm 2 31.4 cm 2 

0.01 cm = 100 µm 5 x 10 -4 µL 1,000,000 0.5 mL 31,400 µm 2 314 cm 2 

0.001 cm = 10 µm 5 x 10 -7 µL 1,000,000,000 0.5 mL 314 µm 2 3,140 cm 2

Cardiac 

Complication No. of Patients No. of Embolic Signals p Value a 

Major 7 392 ... 

Minor 27 183 0.04 

None 48 153 0.01 

a One-way analysisof variance, relative to major cardiac complications. 

i

Length of Stay (days) a 

No. of Embolic Signals All Patients (n = 79) b Neurologic Complications (n = 73) b 

Patients Without Major Cardiac or 

0–100 8.6 ± 2.7 (n = 40) 8.0 ± 2.8 (n = 37) 

101–300 13.5 ± 6.9 (n = 23) 13.7 ± 7.0 (n = 22) 

301–500 16.3 ± 4.8 (n = 10) 15.9 ± 5.1 (n = 9) 

>500 55.8 ± 9.7 (n = 6) 44.8 ± 11.3 (n = 5) 

a 

Data are shown as mean ± standard deviation. b Excludes deaths.



microemboli 




Our studies 


‣Clinical 


in High 

Risk 



‣The 



Novel 


PROJECT DIRECTOR: S. GUNAYDIN, MD, PhD 

CONSULTANTS: K. McCUSKER, CCP, PhD; T. GOURLAY, PhD 

MULTI-CENTER: : T. TEZCANER, MD, Y. ZORLUTUNA, MD 

CHIEF PERFUSIONIST: : T.SARI, Msc 

CELL CULTURE-PHAGOCYTIC INDEX: M.A.ONUR, PhD, A.GURPINAR,PhD; 

P.ATASOY, MD 

SCANNING ELECTRON MICR: M.F.SARGON, MD,PhD 

GENETICS : AYSEN G OZCAN, MD, PhD 

BIOCHEMISTRY: NECATI BINGOL, PhD 

University i of K.Kale-Turkey; 

NY Medical College, NY; University i of Strathclyde-Scotland 

Scotland 

Bayindir Hospital, Hacettepe University/ TURKEY

CLINICAL EVALUATION OF MINIMIZED EXTRACORPOREAL CIRCULATION IN 

HIGH RISK CORONARY REVASCULARIZATION 

Impact on air handling, inflammation, hemodilution and myocardial function 

SERDAR GUNAYDIN, MD 1 ; TAMER SARI, MSc 2 ; KEVIN McCUSKER, CCP, PhD 3 ; 

UWE SCHONROCK, CCP 4 ; YAMAN ZORLUTUNA, MD 2 

1 University of Kirikkale, TURKEY; 2 Bayindir Hospital, TURKEY; 

3 Portsmouth Regional Hospital, NH-USA; 

Klinikum Braunschweig-GERMANY 

4 

Perfusion 2009

PATIENTS & METHODS 

Over a ten-month period, 40 patients (Euroscore 6+) undergoing 

coronary revascularization were prospectively randomized (closed 

envelope allocation) to one of the two perfusion protocols with the 

investigators blinded to the allocation (N=20): 

Group 1: Mini-CPB (Rocsafe MPC, Terumo, USA) 

Group 2: CECC (Capiox SX18, Terumo, USA) 

Blood Sampling 

Baseline: After induction of anesthesia (before administration of 

heparin) (T1) 

Thromboelastography (TEG) control: After heparin administration 

before CPB (T2) 

On CPB: 15 min. after initiation of CPB (T3) 

Off CPB: Before cessation of CPB (before protamine infusion) (T4) 

Protamine: 15 min. after reversal with protamine (T5) 

ICU: First postoperative day at 8:00 a.m. (T6)

GME (emboli.sec -1 ) Group 1 

Group 2 

p 

(Mini-CPB) 

(CECC) 

T3 T4 T3 T4 NS 

Venous (inlet) 32.8±5.3 94.2±8.7 40.4±4.7 107.3±11 NS 

Bubble trap-oxygenator 22.3±4.1 44.3±6 29.3±4.7 51.4±7.1 NS 

Arterial (outlet) 12.6±3.6 18.3±4.6 17.5±4 22.7±4.5 NS

14 

CKMB 

12 

* 

10 

L-1 

ng.m 

8 

6 

Mini-CPB 

CECC 

4 

2 

0 

Pre-CPB 

Post CPB

RFI % Ch hange 

25 

20 

15 

10 

5 

0 

-5 

Neutrophil CD11b/CD18 

* 

* 

T1 T3 T4 T5 T6 

Mini-CPB 

CECC

Utley Award Winner: 

Clinical Performance and 

Biocompatibility of Novel Hyaluronan- 

Coated Heparin-Free Extracorporeal 

Circuits in High-Risk Patients 

Undergoing Coronary Revascularization 

Serdar Gunaydin , Kevin McCusker, 

Tamer Sari, Ibrahim Ucar, Cemi Karabay, 

and Cem Yorgancioglu

In a four-month period, 40 patients (Euroscore 6+ ) were prospectively 

randomized to one of the two perfusion protocols (N=20) 

Group 1: Hyaluronan-coated, heparin free ECC 

(Vision-GBS-HF, Gish, Ca) 

Group 2: Uncoated control 

(Vision-HFO, Gish, Ca) 

 

 

The primary endpoints of this study were to evaluate the air 

handling capacity and to qualify comfort and safety level of novel 

ECC in high risk CABG cases 

Secondary endpoints were to document any differences in contact 

activation- inflammatory response, hemolysis, hemodilution, 

myocardial protection and clinical outcome

GME (emboli.sec 

- 1 ) 

Group 1 

(GBS-COATED) 

Group 2 

(CONTROL) 

p 

T3 

T4 

T3 

T4 

Venous (inlet) 32.8±5.3 

94.2±8.7 

40.4±4.7 

4.7 107.3±11 

11 NS 

Bubble trap-oxygenator 

22.3±4.1 

44.3±6 29.3±4.7 

51.4±7.1 

NS 

Arterial (outlet) 12.6±3.6 

18.3±4.6 

17.5±4 22.7±4.5 

NS

The Impact of the Intensity of Microemboli on 

Postoperative Neurocognitive Outcome in 

Coronary Revascularization 

Serdar Gunaydin, Kevin McCusker, Tamer Sari, 

Yaman Zorlutuna

Microemboli (ME) to cerebral circulation occur 

during CPB and can contribute to 

postoperative neurocognitive dysfunction 

We examined the correlation of the intensity of 

intraoperative microembolic signals with 

respect to inflammatory response, 

postoperative brain perfusion and 

neuropsychological testing in high-risk patients 

undergoing cardiac surgery

Over a two- year period ,ME activity was monitored simultaneously 

during the first and last 15 min. of extracorporeal circulation by fixedbeam 

ultrasonic imaging device detecting and sizing at three locations 

(EDAC, Luna Innovations, Roanoke, VA) and documenting gparticles 

>30 microns in 150 Euroscore 6+ patients 

Patients were randomized into three groups: 

‣ Group 1: those where more than 30 emboli/sec were detected (N=42) 

‣ Group 2: those where 10-30 emboli/sec were detected (N=53) 

‣ Group 3: those where less than 10 emboli/sec(N=55) were detected 

 

 

 

Eight cognitive domains and a global cognitive score, as well as 

depressive and subjective symptoms were analyzed 

Patients underwent Tc99m HMPAO brain SPECT imaging a week 

before and after surgery 

Serum lactate, t interleukin-6 (IL-6),C3a,tumor necrosis factor alpha 

(TNF-alpha), D-dimer and CRP levels were measured. CD11b/CD18 

expressions were determined by flow cytometry

Group 1 had a 33.3% 3% (N=14) rate of neurological 

dysfunction (stroke,coma, delirium or aberrant 

behavior) versus 9.4% (Group 2, N=5) and 5.4% 

(Group3, N=3),detected by neurocognitive 

evaluation(p

Group 1 

Group 2 

Group 3 

(>30emb/s, (10-30 emb/s (

ME intensity is well correlated with 

postoperative neurocognitive outcome in high 

risk patients undergoing CABG 

Early detection of ME can catch accidents and 

errors in technique, and allow the surgical team 

to correct these errors before the problem 

becomes serious

We have designed studies for the evaluation of air handling 

characteristics of minicircuits vs. conventional, air handling evaluation of 

ECC and neurocognitive outcome following high-risk CABG 

We have incorporated ultrasound detection system with cerebral 

oximetry, BIS, TCD, proinflammatory-hematologic l parameters, indicators 

of myocardial preservation, psychological testing and clinical outcome 

Initial results are promising for a perfect correlation with different 

monitoring devices, inflammation and psychological testing 

Online detection systems alert significantly before studied monitoring 

technologies 

 

We believe we have obtained revolutionary data of air embolism of 

significantly higher quantity than expected, based on previous in vitro 

studies 

Ongoing Studies: 

‣ Open vs. closed circuits 

‣ Pulsatile vs. non-pulsatile flow 

‣ Comparison of characteristics of extracorporeal circuits from different 

manufacturers 

‣ Air generation in various procedures



microemboli 




Our studies 


‣Clinical 


in High 

Risk 



‣The 



Novel 


Do we really need air detection 

and count in our clinical 

practice? 

Can we have better clinical 

l 

outcome by better air 

handling?

INTERVENTION 

%DECREASE OF GME DETECTION 

Aortic and venous cannulation 26.2% 

Controlling venous return 52.4% 

Reservoir level correction 18.7% 

Drug administration 69% 

Management of temperature gradient 41% 

Alerting the need of myocardial or 

ventilatory support in post-CPB 

period due to significant air embolism 

QA for different centers and 

perfusionists 

i 25% 

How much GME is important 

t 

clinically?

The total volume of gas tolerated in humans is 

hard to estimate 

Small volumes can lead to symptoms, particularly 

if paradoxical air embolism ensues, potentially 

causing cardiovascular and/or neurological 

problems 

Volumes between 100-300 ml can be fatal 

(approximately 1 mg.kg -1 ) 

This volume is relevant, since it has been shown 

that 100 ml of air per second can be entrained 

through a 14 gauge cannula with only 5 cm 

pressure gradient

Diameter of 

Volume of 

No. of 

Each Bubble Each Bubble Bubbles 

Total Volume 

Surface Area 

of Each 

Bubble 

Total Surface 

Area 

1 cm = 10 mm 05mL 0.5 1 05mL 0.5 314cm 3.14 2 314cm 3.14 2 

0.1 cm = 1 mm 0.5 µL 1,000 0.5 mL 3.14 mm 2 31.4 cm 2 

0.01 cm = 100 µm 5 x 10 -4 µL 1,000,000 0.5 mL 31,400 µm 2 314 cm 2 

0.001 cm = 10 µm 5 x 10 -7 µL 1,000,000,000 0.5 mL 314 µm 2 3,140 cm 2

We believe data obtained via novel air 

detection studies will change the future of 

cardiac surgery 

The amount of air tolerated by humans and the 

definition of post-CPB neurologic dysfunction 

will be redescribed and, following large 

population studies, we can start discussing the 

underestimation of air embolism in patients 

suffering postoperative low cardiac output 

syndrome, renal failure or stroke

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