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

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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

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c la m p s i t e

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% 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)

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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.

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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