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(Patho-)fysiologie van dekransslagader doorbloeding
Patrick Wouters
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Postoperatief myocardinfarct = Belangrijkste
doodsoorzaak na chirurgie 1.3 % in ptn met risico (cardiale complicaties ~ 4 %)
0.3 % in globale populatie (cardiale complicaties ~ 1.5 %)
Hoge Incidentie Ischemische Hartziekte
Ouder wordende populatie
Vaak niet gediagnosticeerd
Intraoperatieve Myocardischemie =
Verhoogd Risico postop myocardinfarct
FACTS
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physiological framework
1. Keeping balance between metabolic supply and demand
= physical laws of hydraulics & oxygen transport
2. Preventing intravascular thrombosis
= Integrity of the endothelium / endovascular wall= Control over coagulation/thrombosis & inflammatory state
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PERFUSION
PRESSURE
DIASTOLIC PHASE
(1/HR)
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Zuurstofaanbod in de coronaircirculatie
zuurstof inhoud(CaO2) x aanbod van bloed (CBF)
A B
A : (1.4 x Hemoglobine x SpO2) + (PaO2 x 0.003)
vb 1.4 x15 g/dl x 100% + 150 mmHg x 0.003
20 ml / 100 ml 0.45 ml
vb 1.4 x 10 x 100 + 600 x 0.003
14 ml / 100 ml 1.8 ml
FFA - lactate - glucose
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Zuurstofaanbod in de coronaircirculatie
zuurstof inhoud(CaO2) x aanbod van bloed (CBF)
A B
B : CBF = CPP / CVR ~ (I = U/R)
250 ml per minuut in rust
kan normaal tot 5 x stijgen bij inspanning
zuurstof extractie is ~ maximaal (in de LV) !
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CPP : drukgradient tussen aorta en ventrikel
Bepaald door :
Diastole ABPLV EDP
en
Diastole duur
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Heart Rate (bmp)
%D
ia
stole
30
30
50 70 90 110 130 150
40
50
60
70
80
EDV
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PERFUSION
PRESSURE
DIASTOLIC PHASE
(1/HR)
PERFUSION
PRESSURE
DIASTOLIC PHASE
(1/HR)
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AoPdiast LVEDP
CVR : wet van Ohm
P R F autoregulation
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pathofysiologie
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Kritische stenose
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PERFUSION
PRESSURE
DIASTOLIC PHASE
(1/HR)
O2 Demand
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Contractility & Relaxation
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Contractility
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Loading conditions
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Nitraten
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POISE Results + Prophylactic
Periop-Blockade
PeriOperative ISchemic Evaluation Trial
190 hospitals, 8351 patients
MI in metoprolol gp vs placebo (4.2 vs 5.7%)BUT :
stroke in metoprolol gp (1.0 vs 0.5%)
mortality in metoprolol gp (3.1 vs 2.3%)
-blockers risk, especially in context of anemia +
hypotension
POISE Study Group; Devereaux PJ, Yang H, et al; Lancet 2008;371:1839-47.
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PERFUSION
PRESSURE SUPPLY DEMAND
General Anesthetics =- sympathetic withdrawal
- mild contractile depression- afterload reduction
SUPPLYDEMAND
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table 4. Hemodynamic Stability from Induction of Anesthesia toOnset of Cardiopulmonary Bypass in 1,012 Patients who
Received Four Different Primary Anesthetics
Anesthesiology 70 ;179-188, 1989
* Totals of columns exceed 100% because some patients had more than one abnormality at the same or different times.
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Anesthesiology 70 ;179-188, 1989
Majority of ischemic events unrelated
to hemodynamic changes !
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Falk et al, 1995
0
20
40
60
80
100
68%
18%
14%>70%
5070%
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Shear Stress
Inflammation
Plaque ruptureConsolidation
Natural Healing
Process
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Pathophysiology of Acute Coronary Syndromes
Balancing the Stability Equation
Repair ThrombosisInflammation
Stable Plaque Unstable Plaque
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perioperative myocardial infarction
acute coronary thrombosis myocardial ischemia
inflammation hypercoagulability stress tissue hypoxemia
plaquefissuring
increasedcatecholamine+ cortisol levels
oxygendelivery
plaquefissuring
coronary arteryshear stress increase in
blood pressureand heart rate
oxygendemand
surgery anesthesia
surgery anesthesia
hypothermia anemiapain
hypotension hypoxemia hypervolemia tachycardia anemia
Courtesy of S. De Hert
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N Engl J Med, Vol. 347, No. 17
ASPIRIN AND MORTALITY FROM CORONARY BYPASS
SURGERY
MANGANO & MULTICENTER STUDY OF PERIOPERATIVE ISCHEMIA RESEARCHGROUP
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Aspirin withdrawal
- Hyperaggregability
- Reduced fibrinolysis
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de Souza DG, Baum VC, Ballert NM: Late thrombosis (> 1 year) of
a drug-eluting stent presenting in the perioperative period.
ANESTHESIOLOGY 2007; 106:10579
A i i fl
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Anti-inflammatory treatment
Statins
JAMA. 2004 May 5;291(17):2092-9
J Vasc Surg 2004;39:967 : RCT statins > 2 weeks preop = 3.1 fold reduction CVE
n = 780.000
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Reduce lipid accumulation
Reduce inflammatory cell infiltration
into plaques
Accumulation of modified lipid
Endothelial cell activation
Inflammatory cell migration
Inflammatory cell activation
VSMC recruitment
VSMC proliferation and matrix synthesis
Fibrous cap formation
Plaque rupture
Platelet aggregation
Thrombosis
Inhibit platelet aggregation
Pleiotropic effects of Statins
Reduce blood thrombogenicity
Normalize endothelial cell function
Effects on VSMC
proliferation and matrix
synthesis
differ between statins
Perioperative ischemia
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A change of paradigm
from hydraulic model tothe vulnerable plaquemodel
Current Diagnostic methods fail to fully assess risk
Managing Oxygen supplydemand is insufficient to preventMI
Treatment strategies should focus on control of
Inflammation Thrombosis
Reduction of Shear Stress
e ope at e sc e a
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To remember
Hemodynamic management :
Preserve diastolic perfusion pressure
no tachycardia
Avoid hypoxia, extreme anemia (?)
Non-hemodynamic related ischemia :
beta blockade and stress prevention (pain-shivering)
Postoperative Anti-thrombosis
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The ischemic syndromes
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The wavefront phenomenon of
Acute Myocardial Infarction
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Myocardial Stunning : temporary reversible dysfunction
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Myocardial Stunning
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Myocardial Hibernation : persistent (but reversible ?)
dysfunction
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Ischemia
Imbalanced
Progressive
Inotropes harmful
Stunning
Balanced
Progressive
Inotropes Useful
Hibernation
BalancedSlowly Progressive
Inotropes harmful
at high dose
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Myocardial Protection
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5
10
15
20
25
30
35
Infarctsize
(%
ofareaatrisc)
O1
.5
.10
.15
.20
.25
.30
.35
C
ollateralFlow
(ml/min.gm)
O2 O3 O4
R1 R2 R3 R4
40 ' OCCLUSION
40 ' OCCLUSION
Preconditioned
Control
day 4
Murry et al. Circulation 1986
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Anesthesiology 1999; 91:1437-46
M h i A th ti
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Mechanisms Anesthetic
PreconditioningTriggersMediatorsEffectors
TM
E
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