London, OntarioCANADA
John M Murkin MD,FRCPC
Director of Cardiac Anesthesiology Research
Professor of Anesthesiology
Schulich School of Medicine
University of Western Ontario
London, Ontario, Canada
Optimizing Bypass for End-Organ Preservation:
Beyond mini-CPB
Disclosures (2 years): Hutchinson: equipment supportSafeOp Surgical: Scientific Advisory BoardOrnim Medical: Scientific Advisory Board, lecture
honoraria, equipment supportPSI Ontario: 3 year peer reviewed grant
Disclosures (5 years): Somanetics/Covidien lecture honoraria, equipment
support Heart and Stroke 3 year peer reviewed grantFoundation
Rbc txInotropic supportPeak troponin
CABG, AVRMortalityPostop MIPostoppostop a fibPeak troponinInotropic support Rbc transfusion
COMICScCPB vs MiECC
randomized trial
Suggestive of MiECC antiinflammatory?
•Aortic instrumentation?•Cannula design?•NIRS end organ
perfusion?•Oximetry guided
transfusion?
1800 patientsCAD: 3 vessel or LMCArandomized PCI vs CABG
SYNTAX Trial
Why ↑ CVA with cardiac surgery?
Mechanisms of Perioperative End Organ Injury
Atherosclerotic emboli
Hypoperfusion
Panvascular Inflammation (unstable
plaque)
CNS Injury: Aortic Instrumentation
472 patients epiaortic scanning pre/post cannulation CPB
Overall 2.1% incidence CNS
complications
New Aortic lesions: 3.4% (16)
Atheroma < 3mm: 0.8%
Atheroma 3-4 mm: 11.8%
Atheroma > 4 mm: 33.3%
Caveat: Aortic Clamping
Severe intimal tear/flapn =10: 6 d/t aortic clamping 4 d/t cannulation
30% (3/10) postop CVA
Caveat: Aortic Clamping
Early/delayed CVA?CNS Injury: Aortic Instrumentation
Intimal tear: secondary thrombus, plaque emboli,
Mechanism of later postoperative CVA?
ASA-associated decrease in postoperative CVA? (NEJM 2004)
Peer review funding HSFO
1 3 . 7
2 1 . 5
1 6 . 7
6 . 8
2 3 . 5
0
5
1 0
1 5
2 0
2 5
C a n n u la s i t e A o r t i c X -
c la m p s i t e
C a n n u la
T y p e
P a r t ia l
c la m p s i t e
O v e r a l l
% o f E p ia o r t ic S c a n P a t ie n t s w it h
C h a n g e in S u r g ic a l M a n a g m e n t
(N = 102)
V
0
5
10
15
20
25
30
35
40
45
50
Cannulation on CPB X-clamp on X-clamp off S-C on S-C off Decannulation Total
TCD Emboli Counts
aortic palpation
epiaortic scan
* * ***
N = 102 scan
N = 109 palpation
(* p <0.05)
Significant reduction in cerebral emboli
associated with epiaortic scanning with
overall reduction incerebral embolic load.
*
Evidence Based Mechanisms
of CNS Injury: Macroemboli
Epiaortic ScanNon-calcific soft plaque
(24/102 patients unrecognized plaque)
EAS: Alter Surgical Approach
Cannulation: distal archSCA
Cannula: dispersion tip
Clamp: single occlusion0 clamp (pump
assist CAB)
TCD emboli significantly less
with distal aortic arch cannulation vs ascending aorta(J Thorac Cardiovasc Surg 1999;118:740-5)
CNS Injury: CABG vs OPCAB(partial occlusion clamp(s)?)
Aortic Side Clamp
Retrospective review, 4875 patients:
CABG n = 2830,
OPCAB n = 1993 (± ASC): +ASC = 460, -ASC = 1533
Clinical CVA = 1.0%
(24 early, 25 delayed)
CVA: off-pump + ASC = CABG
“Aortic manipulation must be avoided in patients with extracoronary vasculopathy”
OPCAB aortic U/S Epiaortic ScanNo EAS: 1019 y/n partial clamp (31.9% / 68.9%)EAS: 1273 (23.7% / 76.3%)
“in subgroup of patients with EAS and partial aortic clamp the incidence of early stroke was significantly lower”
2.8% (9/317) vs 0.7% (2/301)
Case control 2002-2009N = 141 CVA vs 565 no CVA
CPB:CVA single vs double clamp (OR 0.385, p = 0.044)
Trends:EAS: 45.3% to 89.4%Side Clamp: 97.7% to 72.7%
EAS
What is current rate of EAS or TEE screening +/- EAS??
very low……
Aortic Instrumentation
• TEE +/- EAS
• TEE if no significant plaque descending aorta (≤ Gr II)
• EAS using TEE surface probe in sterile sheath
Standard cannula: velocity 1 cm from tip > 400 cm/sec
Normal peak velocity in human aorta 80 cm/sec
There is on average a 500% increase in flow velocity
within the aorta during CPB with a conventional aortic cannula
Sarns Soft Flow: velocity 1 cm from tip 100 cm/sec
Normal peak velocity in human aorta 80 cm/sec
Baxter RMI Dispersion cannula: force < 80% of regular tip
Aortic Instrumentation
Mechanisms of Perioperative End Organ Injury
Atherosclerotic emboli
Hypoperfusion
Panvascular Inflammation (unstable
plaque)
What is optimal MAP during CPB???
Can now detect and individualize MAP (end organ perfusion
pressure):
?Improved outcomes?
{
Cerebral Autoregulation (dynamic)
dynamic Cerebral Autoregulation (dCA):‘beat –to –beat’ coherence analysis:
MAP vs ICP→ MAP vs TCD→ MAP vs ScO2→ MAP vs NIRS_CBF
N=234 CPBCorrelation: TCD/NIRS vs MAP
Impaired cerebral autoreg
CVA: 6/47 (12.8%)
65/187 (2.7%)
Dynamic cerebral autoregulation
Detect LLA, thresholdfor MAP, AUC <LLA associatedend organ failure
LLA
N = 450 CABG/valveNIRS/MAP: dynamic cerebral autoregulation(no interventions)
Below cerebral autoregulation:83/450 major morbidity, mortality (MOMM 18.2%)
AUC (MAP x min) independently associated MOMMCI: 1.08-1.71 (p=0.008)
Cerebral desaturation associated with adverse outcomes,Intervention improves outcomes.
10
4
1
4
1 1 1 10 0 0
11
3
Death >48
Ventilation
Mediastinitis Combined
Outcomes*
STS Major Morbidity Mortality
Control
INVOS
Combined outcomes:p = 0.024
CVA
*
MOMM
Does cerebral autoregulation (LLA) encompass renal autoregulation?
AUC < LLA
Not: if brain OK everything OK…rather
If brain not OK then beware and BE AWARE!
NIRS for transfusion / perfusion monitoring
Cerebral NIRS
NIRS tissue perfusion
Low Hct (< 24%) good NIRS rSO2 (~ basal)≈ no transfusion
Microcirculation???
NIRS VOT PARAMETERS
(TISSUE OXIMETRY ISCHEMIA/REPERFUSION CHALLENGE)
Baseline
Rate of deoxygenation(tissue metabolism)
Rate of reoxygenation
Endothelial vasoreactivity
Progressive decrease microvascular vasoreactivity during non-pulsatile CPB
Does failure to normalize VOT indicate organ dysfunction postop?
Mechanisms of Perioperative CNS Injury
Atherosclerotic emboli
Hypoperfusion
Panvascular Inflammation (unstable
plaque)
Unstable angina= ↑ stroke risk
CABG patients: Unstable vs stable angina
N = 273 retrospective + 92 prospective
64% incidence carotid plaque
Unstable angina:CRP sig higher ∝ ‘complex’ plaque
Carotid stenosis ‘complex/ulcerated’23.2% unstable vs 3.2% stable
‘Activation’ of carotid plaque
n=10 awaiting CABG (asymptomatic carotid)
n=10 asymptomatic control carotid disease (risk factors)
MRI assessment of carotid plaque
Quantification of T2 attenuation
CABG
asymptomatic
Angina (CABG) patients had less carotid stenosis(XSA) yet greater inflammatory activity (94%) in carotid plaque vs asymptomatic cohort (24%)
Angina patients have activation of diffuse (non-coronary) plaque thus less reserve for further insult (eg. emboli, hypoperfusion, wbc activation etc)
MiECC vs cCPB???
N = 1046 OPCABDaily CRP, statin use
Max CRP ~ lactate, BE
MOMM ~ CRPStatin lower MOMM
Panvascular inflammation
•?more aggressive antiinflammatorystrategies
•Better characterization of individual susceptibility
Are adverse CNS and systemic events inevitable?
orcan we mitigate?
Summary:
Epiaortic scan
Single cross clamp (prox anastamoticdevice, skip graft etc.)
NIRS: perfusion, transfusion, ?cerebral autoregulation?
+Antiinflammatory strategies (ASA, statins, biocompatible ECC)
Lacus Nostri, Harrington, Ontario
