beyond mini-cpb london, ontario canada john m murkin … · london, ontario canada john m murkin...
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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
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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
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Rbc txInotropic supportPeak troponin
CABG, AVRMortalityPostop MIPostoppostop a fibPeak troponinInotropic support Rbc transfusion
COMICScCPB vs MiECC
randomized trial
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Suggestive of MiECC antiinflammatory?
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•Aortic instrumentation?•Cannula design?•NIRS end organ
perfusion?•Oximetry guided
transfusion?
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1800 patientsCAD: 3 vessel or LMCArandomized PCI vs CABG
SYNTAX Trial
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Why ↑ CVA with cardiac surgery?
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Mechanisms of Perioperative End Organ Injury
Atherosclerotic emboli
Hypoperfusion
Panvascular Inflammation (unstable
plaque)
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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
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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)
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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.
*
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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)
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TCD emboli significantly less
with distal aortic arch cannulation vs ascending aorta(J Thorac Cardiovasc Surg 1999;118:740-5)
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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”
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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)
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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
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What is current rate of EAS or TEE screening +/- EAS??
very low……
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Aortic Instrumentation
• TEE +/- EAS
• TEE if no significant plaque descending aorta (≤ Gr II)
• EAS using TEE surface probe in sterile sheath
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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
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Mechanisms of Perioperative End Organ Injury
Atherosclerotic emboli
Hypoperfusion
Panvascular Inflammation (unstable
plaque)
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What is optimal MAP during CPB???
Can now detect and individualize MAP (end organ perfusion
pressure):
?Improved outcomes?
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{
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
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N=234 CPBCorrelation: TCD/NIRS vs MAP
Impaired cerebral autoreg
CVA: 6/47 (12.8%)
65/187 (2.7%)
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Dynamic cerebral autoregulation
Detect LLA, thresholdfor MAP, AUC <LLA associatedend organ failure
LLA
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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)
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Cerebral desaturation associated with adverse outcomes,Intervention improves outcomes.
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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
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Does cerebral autoregulation (LLA) encompass renal autoregulation?
AUC < LLA
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Not: if brain OK everything OK…rather
If brain not OK then beware and BE AWARE!
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NIRS for transfusion / perfusion monitoring
Cerebral NIRS
NIRS tissue perfusion
Low Hct (< 24%) good NIRS rSO2 (~ basal)≈ no transfusion
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Microcirculation???
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NIRS VOT PARAMETERS
(TISSUE OXIMETRY ISCHEMIA/REPERFUSION CHALLENGE)
Baseline
Rate of deoxygenation(tissue metabolism)
Rate of reoxygenation
Endothelial vasoreactivity
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Progressive decrease microvascular vasoreactivity during non-pulsatile CPB
Does failure to normalize VOT indicate organ dysfunction postop?
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Mechanisms of Perioperative CNS Injury
Atherosclerotic emboli
Hypoperfusion
Panvascular Inflammation (unstable
plaque)
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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
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‘Activation’ of carotid plaque
n=10 awaiting CABG (asymptomatic carotid)
n=10 asymptomatic control carotid disease (risk factors)
MRI assessment of carotid plaque
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Quantification of T2 attenuation
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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???
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N = 1046 OPCABDaily CRP, statin use
Max CRP ~ lactate, BE
MOMM ~ CRPStatin lower MOMM
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Panvascular inflammation
•?more aggressive antiinflammatorystrategies
•Better characterization of individual susceptibility
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Are adverse CNS and systemic events inevitable?
orcan we mitigate?
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Summary:
Epiaortic scan
Single cross clamp (prox anastamoticdevice, skip graft etc.)
NIRS: perfusion, transfusion, ?cerebral autoregulation?
+Antiinflammatory strategies (ASA, statins, biocompatible ECC)
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Lacus Nostri, Harrington, Ontario