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IntraoperativeIntraoperative
Myocardial ProtectionMyocardial Protection
PRESENTORPRESENTOR ±± Dr. Sameer goyal Dr. Sameer goyal
MODERATORMODERATOR ±± Dr. S.K. Mathur Dr. S.K. Mathur
Dr. R.K Dubey Dr. R.K Dubey
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Cardiac PhysiologyCardiac Physiology
Myocardium requires continuous supply of o2.Myocardium requires continuous supply of o2.
Ischemia occurs when demand > supply.Ischemia occurs when demand > supply.
Myocardial o2 supply depends on:Myocardial o2 supply depends on:
a) arterial o2 contenta) arterial o2 content
o2 content = (Hb) 1.34 (% saturation) + .003(Po2)o2 content = (Hb) 1.34 (% saturation) + .003(Po2)
b) flow of oxygenated blood to myocardium i.e.b) flow of oxygenated blood to myocardium i.e.
CBF.CBF.
Blood flow to subendocardium occurs duringBlood flow to subendocardium occurs during
diastole. Most vulnerable to ischemia.diastole. Most vulnerable to ischemia.
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O2 delivery may be insufficient because of either:O2 delivery may be insufficient because of either:
a)a) in perfusion pressure ( systemicin perfusion pressure ( systemic
hypotension, CAD )hypotension, CAD )
b)b) in ventricular end diastolic pressure ( aorticin ventricular end diastolic pressure ( aortic
stenosis, VF, ventricular distension etc).stenosis, VF, ventricular distension etc).
Myocardial O2 consumptionMyocardial O2 consumption
1) normal beating heart = 8ml/ 100gms/ min1) normal beating heart = 8ml/ 100gms/ min
2) empty beating heart = 5.6ml/ 100gms/ min2) empty beating heart = 5.6ml/ 100gms/ min
3) arrested heart = 1.1ml/ 100gms/ min3) arrested heart = 1.1ml/ 100gms/ min
4) cooling to 22C = .3ml/ 100gms/ min4) cooling to 22C = .3ml/ 100gms/ min
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Events during CPB that may lead toEvents during CPB that may lead to
myocardial injurymyocardial injury
Aortic cross clamping,Aortic cross clamping,
VF,VF,
Ventricular distension,Ventricular distension,
Coronary embolism,Coronary embolism,
Low perfusion pressure,Low perfusion pressure,
Catecholamines,Catecholamines,
ReperfusionReperfusion
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Mechanism of myocardial ischemic injuryMechanism of myocardial ischemic injury
Depletion of high energy phosphates,Depletion of high energy phosphates,
Intracellular acidosisIntracellular acidosis
Alteration in Calcium homeostasis,Alteration in Calcium homeostasis,
O2 free redicals,O2 free redicals,
Complement activation.Complement activation.
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AORTIC CROSS CLAMPAORTIC CROSS CLAMP
PROBLEMS WITH NORMOTHERMIC ISCHEMIC ARRESTPROBLEMS WITH NORMOTHERMIC ISCHEMIC ARREST
�� PERSISTENT ELECTRICAL AND MECHANICAL ACTIVITYPERSISTENT ELECTRICAL AND MECHANICAL ACTIVITY
DURING MUCH OF THE ISCHEMIC PERIOD DEPLETESDURING MUCH OF THE ISCHEMIC PERIOD DEPLETES
HIGH ENERGY PHOSPHATE AND COMPROMISES POSTHIGH ENERGY PHOSPHATE AND COMPROMISES POST--
REPAIR VENTRICULAR PERFORMANCEREPAIR VENTRICULAR PERFORMANCE
�� SAFE ISCHEMIC TIME INSUFFICIENT TO COMPLETESAFE ISCHEMIC TIME INSUFFICIENT TO COMPLETE
MOST REPAIRSMOST REPAIRS
�� INTERMITTENT CROSS CLAMP WITH PERIODS OFINTERMITTENT CROSS CLAMP WITH PERIODS OF
REPERFUSION DOES LITTLE TO IMPROVE OPERATINGREPERFUSION DOES LITTLE TO IMPROVE OPERATING
CONDITIONS OR PREVENT MYOCARDIAL NECROSIS.CONDITIONS OR PREVENT MYOCARDIAL NECROSIS.
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RAPID CESSATION OF ELECTRORAPID CESSATION OF ELECTRO--MECHANICALMECHANICAL
ACTIVITY FOLLOWING CROSS CLAMP DESIRABLEACTIVITY FOLLOWING CROSS CLAMP DESIRABLE
BOTH FOR EXPOSURE AND MYOCARDIALBOTH FOR EXPOSURE AND MYOCARDIAL
PRESERVATIONPRESERVATION
DIFFERENCES IN MYOCARDIAL VULNERABILITYDIFFERENCES IN MYOCARDIAL VULNERABILITY
MAKE IT IMPOSSIBLE TO PREDICT A µSAFE¶ MAKE IT IMPOSSIBLE TO PREDICT A µSAFE¶
PERIOD OF ISCHEMIAPERIOD OF ISCHEMIA
EXTENT OF NECROSIS IS DIRECTLYEXTENT OF NECROSIS IS DIRECTLY
PROPORTIONAL TO THE DURATION OF AORTICPROPORTIONAL TO THE DURATION OF AORTIC
CROSS CLAMPCROSS CLAMP
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PATHOPHYSIOLOGY OF GLOBALPATHOPHYSIOLOGY OF GLOBAL
MYOCARDIAL ISCHEMIAMYOCARDIAL ISCHEMIA
qq HIGH ENERGYHIGH ENERGYPHOSPHATEPHOSPHATEPRODUCTIONPRODUCTION
PERSITENT HIGH ENERGY
PHOSPHATE UTILIZATION
DECREASED HIGH ENERGY
PHOSPHATEAVAILABILITY
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DURING ISCHEMIA, THE MAIN SOURCES OF HIGH ENERGYDURING ISCHEMIA, THE MAIN SOURCES OF HIGH ENERGY
PHOSPHATE ARE CREATINE PHOSPHATE AND ANAEROBICPHOSPHATE ARE CREATINE PHOSPHATE AND ANAEROBICPRODUCTION OF ATPPRODUCTION OF ATP
ANAEROBIC PRODUCTION OF ATP IS SELFANAEROBIC PRODUCTION OF ATP IS SELF-- LIMITEDLIMITED
BECAUSE OF ACCUMULATION OF METABOLITES SUCH ASBECAUSE OF ACCUMULATION OF METABOLITES SUCH AS
LACTATE, PYRUVATE AND PROTONS, WHICH EVENTUALLYLACTATE, PYRUVATE AND PROTONS, WHICH EVENTUALLY
INHIBIT ESSENTIAL ENZYME SYSTEMSINHIBIT ESSENTIAL ENZYME SYSTEMS
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CP AND ATP LEVELS DECLINE RAPIDLY FOLLOWINGCP AND ATP LEVELS DECLINE RAPIDLY FOLLOWING
GLOBAL ISCHEMIA BECAUSE OF PERSISTENT ENERGYGLOBAL ISCHEMIA BECAUSE OF PERSISTENT ENERGY
UTILIZATION FOR ELECTROMECHANICAL AND BASALUTILIZATION FOR ELECTROMECHANICAL AND BASAL
METABOLIC ACTIVITYMETABOLIC ACTIVITY
PROLONGED ISCHEMIA RESULTS IN SEVERE MYOCARDIALPROLONGED ISCHEMIA RESULTS IN SEVERE MYOCARDIAL
CONTRACTURECONTRACTURE
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ENERGY UTILIZATION IS CLOSELY LINKED TO MOVEMENT OFCALCIUM IONS
TRANSPORT OF CALCIUM INTO THE MYOCYTE(CONSUMES LITTLE ENERGY)
RISE IN INTRACELLULAR CALCIUM TRIGGERS ASERIES OF REGULATORY REACTIONS RESULTING
IN MYOCARDIAL CONTRACTION AND ENERGY
UTILIZATION
ENERGY DEPENDENT TRANSPORT OF
CALCIUM TO OUTSIDE THE CELL FOR
MYOCARDIAL RELAXATION
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LOW PRODUCTION OF
ATP DUE TO ANAEROBIC
METABOLISM
INCREASED CYTOSOLIC
CONCENTRATION OF IONIZED
CALCIUM
FORMATION OF RIGOR
BONDS BETWEEN
CONTRACTILE
PROTEINS WITH
PERSISTENT ENERGYUTILIZATION
INCREASED
PRODUCTION AND
ACCUMULATIONOF H+ IONS AND
FREE FATTY ACIDS
RELEASE OFINTRACELLULAR
LIPOPROTEIN LIPASE
LOSS OF CELL
INTEGRITY AND
FUNCTION
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Consequences of ischemia and reperfusion injuryConsequences of ischemia and reperfusion injury
Depends on length of ischemia,Depends on length of ischemia,
temp. of myocardium,temp. of myocardium,
Myocardial stunningMyocardial stunning: represents viable: represents viable
myocardium having systolic/diastolic dysfunctionmyocardium having systolic/diastolic dysfunction
in the presence of normal myocardial perfusion.in the presence of normal myocardial perfusion.
* complete functional recovery.* complete functional recovery.
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Hybernating myocardium:Hybernating myocardium: viable myocardiumviable myocardium
that is chronically underperfused and hasthat is chronically underperfused and has
downregulated its contractile functions.downregulated its contractile functions.
* On reperfusion, returns to normal function.* On reperfusion, returns to normal function.
Myocardial necrosisMyocardial necrosis : myocytes irreversibly: myocytes irreversibly
injuredinjured
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Intervention before the onset of ischemiaIntervention before the onset of ischemia
A)A) Minimization of ongoing ischemiaMinimization of ongoing ischemia::
* by use of nitrates, anticoagulants, antiplatelet agents,* by use of nitrates, anticoagulants, antiplatelet agents,
* insertion of IABP in the perioperative period,* insertion of IABP in the perioperative period,
* controlling HTN, tachycardia, pt. anxiety,* controlling HTN, tachycardia, pt. anxiety,
* use of supplemental O2.* use of supplemental O2.
B)B) Perioperative ßPerioperative ß--blokadeblokade::
* unless contraindicated,* unless contraindicated, cardiac related mortility.cardiac related mortility.
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C)C) Rapid revascularizationRapid revascularization
D)D) Fibrillary arrestFibrillary arrest : creates a nearly motionless heart,: creates a nearly motionless heart,
: either through electrical stimulation or: either through electrical stimulation or
myocardial cooling.myocardial cooling.
1) Normothermic fibrillary arrest :1) Normothermic fibrillary arrest :
: by placing alternating current generator in contact: by placing alternating current generator in contact
with ventricular myocardium.with ventricular myocardium.
: ventricle remain in fibrillation with little ventricular: ventricle remain in fibrillation with little ventricular
motion.motion.
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Disadv. :Disadv. :
1) energy consumption is high as myocardium is warm1) energy consumption is high as myocardium is warm
and in a state of continuous contraction.and in a state of continuous contraction.
2)2) wall tension.wall tension.
3) endocardial perfusion compromised due to aabsence3) endocardial perfusion compromised due to aabsence
of diastole.of diastole.
Not recommendedNot recommended
2) Hypothermic fibrillary arrest : energy consumption is less2) Hypothermic fibrillary arrest : energy consumption is less
but not as low as complete arrestbut not as low as complete arrest
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Prevention of ventricular distentionPrevention of ventricular distention
CAUSES INCREASED MYOCARDIAL WALL TENSION ANDCAUSES INCREASED MYOCARDIAL WALL TENSION AND
MVOMVO22
REDUCES SUBENDOCARDIAL PERFUSION DUE TOREDUCES SUBENDOCARDIAL PERFUSION DUE TO
INCREASED INTRACAVITY PRESSUREINCREASED INTRACAVITY PRESSURE
POTENTIATED BYPOTENTIATED BY
�� INADEQUATE VENOUS RETURNINADEQUATE VENOUS RETURN
�� AORTIC INSUFFICIENCYAORTIC INSUFFICIENCY
�� VFVF
�� INCREASED PV RETURN AND NONCORONARYINCREASED PV RETURN AND NONCORONARY
COLLATERAL FLOW IN THE QUIESCENT HEARTCOLLATERAL FLOW IN THE QUIESCENT HEART
�� POSTPOST--REPAIR CARDIAC FAILUREREPAIR CARDIAC FAILURE
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STRATEGIES TO PREVENT VENTRICULARSTRATEGIES TO PREVENT VENTRICULAR
DISTENSIONDISTENSION
OPTIMIZE VENOUS DRAINAGEOPTIMIZE VENOUS DRAINAGE
OPTIMIZE CPB FLOW RATESOPTIMIZE CPB FLOW RATES
VENT THE LEFT HEARTVENT THE LEFT HEART
EARLY DEFIBRILLATIONEARLY DEFIBRILLATION
EARLY CROSS CLAMPING IN AORTICEARLY CROSS CLAMPING IN AORTIC
INCOMPETENCEINCOMPETENCE
VASODILATORS MAY HELP SOMETIMESVASODILATORS MAY HELP SOMETIMES
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Myocardial PreconditioningMyocardial Preconditioning
DEFINED ASDEFINED AS THE CONCEPT OF ENDOGENOUS ADAPTATION THE CONCEPT OF ENDOGENOUS ADAPTATION
TO SUBLETHAL GLOBAL ISCHEMIA RESULTING IN TO SUBLETHAL GLOBAL ISCHEMIA RESULTING IN
PROTECTION AGAINST A LONGER LETHAL ISCHAEMIC PROTECTION AGAINST A LONGER LETHAL ISCHAEMIC
EPISODE EPISODE
HAS BEEN DEMONSTRATED EXPERIMENTALLY IN ANIMALHAS BEEN DEMONSTRATED EXPERIMENTALLY IN ANIMAL
HEARTS, AND ALSO IN CLINICAL CIRCUMSTANCES INHEARTS, AND ALSO IN CLINICAL CIRCUMSTANCES INHUMANS IN A FEW STUDIESHUMANS IN A FEW STUDIES
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POSSIBLE MECHANISMS OFPOSSIBLE MECHANISMS OF
PRECONDITIONINGPRECONDITIONING
INITIALLY THOUGHT TO BE DUE MANIFESTATION OF INCREASEDINITIALLY THOUGHT TO BE DUE MANIFESTATION OF INCREASED
COLLATERAL FLOWCOLLATERAL FLOW
PRESENT RESEARCH HYPOYHETISES THE EFFECTS TO BEPRESENT RESEARCH HYPOYHETISES THE EFFECTS TO BE
MEDIATED BY ADENOSINE AND A SIGNAL TRANSDUCTIONMEDIATED BY ADENOSINE AND A SIGNAL TRANSDUCTION
PATHWAY INVOLVING GPATHWAY INVOLVING G--PROTEINS, A PHOSPHOLIPASE ANDPROTEINS, A PHOSPHOLIPASE AND
PROTEIN KINASE C (PKC)PROTEIN KINASE C (PKC)
ANOTHER HYPOTHESIS INVOLVED ATPANOTHER HYPOTHESIS INVOLVED ATP--DEPENDANT KDEPENDANT K++
CHANNELSCHANNELS
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SHOWN TO HAVE MAXIMUM BENEFIT WHEN THE ISCHEMICSHOWN TO HAVE MAXIMUM BENEFIT WHEN THE ISCHEMIC
PERIOD IS A SINGLE EPISODE OF 3PERIOD IS A SINGLE EPISODE OF 3 -- 5 MINS, ABOUT 35 MINS, ABOUT 3 -- 5 MINS5 MINS
PRIOR TO THE PROLONGED ISCHEMIC PERIODPRIOR TO THE PROLONGED ISCHEMIC PERIOD
THE BENEFITS WEAR OFF BEYOND ABOUT 2 HOURS OFTHE BENEFITS WEAR OFF BEYOND ABOUT 2 HOURS OF
PROLONGED ISCHEMIAPROLONGED ISCHEMIA
BENEFITS SEEN MAXIMALLY WITH LIMITING INFARCT SIZE ANDBENEFITS SEEN MAXIMALLY WITH LIMITING INFARCT SIZE AND
ARRHYTHIAS AFTER THE ISCHEMIC PERIODARRHYTHIAS AFTER THE ISCHEMIC PERIOD
HAS NOT BEEN SHOWN TO HAVE SIGNIFICANT BENEFITS INHAS NOT BEEN SHOWN TO HAVE SIGNIFICANT BENEFITS IN
DECREASING MYOCARDIAL STUNNING RELATED LOW CARDIACDECREASING MYOCARDIAL STUNNING RELATED LOW CARDIAC
OUTPUTOUTPUT
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Stimuli producing preconditioning response:Stimuli producing preconditioning response:
: ischemia,: ischemia,
: drugs ( bradykinin, phenylephrine,: drugs ( bradykinin, phenylephrine,
endotoxin, adenosine)endotoxin, adenosine)
: inhalational anaesthetic agents(: inhalational anaesthetic agents(
sevoflurane, desflurane, isoflurane).sevoflurane, desflurane, isoflurane).
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Interventions during ischemiaInterventions during ischemia
A)A) Myocardial tempr.Myocardial tempr.
1) Hypothermia: myocardial O2 consumption1) Hypothermia: myocardial O2 consumption
by 50% for every 10Cby 50% for every 10C in myocardialin myocardial
tempr. Cooling produced through:tempr. Cooling produced through:
a) cold cardioplegia : given at 4C to 10C anda) cold cardioplegia : given at 4C to 10C and
produce myocardial cooling to 15C to16C.produce myocardial cooling to 15C to16C.
b) topical cooling : chilled saline or slushb) topical cooling : chilled saline or slush
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2) Warm cardioplegia : metabolic activity continues2) Warm cardioplegia : metabolic activity continues
but at a lesser degree because mechanicalbut at a lesser degree because mechanicalactivity of heart is abolished.activity of heart is abolished.
a) supplied continuously to avoid ischemic injury.a) supplied continuously to avoid ischemic injury.
b) lower postop incidence of low output state.b) lower postop incidence of low output state.
c) use of blood cardioplegia which carry enough O2c) use of blood cardioplegia which carry enough O2
to meet demands of warm myocardium.to meet demands of warm myocardium.
d) may not provide adequte protection in presenced) may not provide adequte protection in presence
of severe CAD.of severe CAD.
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3) Tepid cardioplegia :3) Tepid cardioplegia :
: administerd at 29C,: administerd at 29C,
: provide some benefits of warm cardiplegia: provide some benefits of warm cardiplegia
while minimizing effects of hypothermia onwhile minimizing effects of hypothermia on
myocardium.myocardium.
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Purpose of cardioplegiaPurpose of cardioplegia
�� Objective is to stop the heart as quickly asObjective is to stop the heart as quickly aspossible to enjoy the benefits of a quiet,possible to enjoy the benefits of a quiet,
bloodless operative field while minimisingbloodless operative field while minimising
ischaemic injury to the heartischaemic injury to the heart�� Cold chemical cardioplegia provides betterCold chemical cardioplegia provides better
protection than cold ischaemic arrestprotection than cold ischaemic arrest
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Hypothermia potentiates the protective effects of Hypothermia potentiates the protective effects of
chemical cardioplegiachemical cardioplegia
�� Ideal cardioplegic solution should eliminateIdeal cardioplegic solution should eliminate
external cardiac work by inducing diastolic arrest,external cardiac work by inducing diastolic arrest,
minimize myocardial oxygen requirements andminimize myocardial oxygen requirements and
cause no myocardial damage itself cause no myocardial damage itself
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Ions & BuffersIons & Buffers
�� The solution should be slightly hypertonicThe solution should be slightly hypertonic
(315(315--350 mOsm/l) to minimize myocardial350 mOsm/l) to minimize myocardial
oedemaoedema
�� Cardioplegia solutions are buffered so as toCardioplegia solutions are buffered so as to
maintain an alkaline pH; as at 37maintain an alkaline pH; as at 37°°C the neutralC the neutral
pH of water is 6.8, at 0pH of water is 6.8, at 0°°C it rises to 7.5,C it rises to 7.5,
therefore require to maintain an alkalinetherefore require to maintain an alkaline
solution if neutrality is maintained [ie a pHsolution if neutrality is maintained [ie a pH
of 6.8 while hypothermic is acidic which mayof 6.8 while hypothermic is acidic which may
cause ischaemic myocardial damage]cause ischaemic myocardial damage]
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Composition of CardioplegiaComposition of Cardioplegia
SolutionsSolutions
Two types:Two types:
1) Crystalloid cardioplegia :1) Crystalloid cardioplegia :
: do not contain Hb,: do not contain Hb,
: deliver dissolved O2 only,: deliver dissolved O2 only,
: small amount of O2 is adequate at cold: small amount of O2 is adequate at cold
tempr. But insufficient in warm myocardium.tempr. But insufficient in warm myocardium.
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2)2) Blood cardioplegia : produced by mixing blood toBlood cardioplegia : produced by mixing blood to
crystalloid in adefinite ratio, with a final Hct. Of crystalloid in adefinite ratio, with a final Hct. Of
16 to 20%.16 to 20%.
�� improved oxygen carrying capacity and deliveryimproved oxygen carrying capacity and delivery
until electromechanical quiescence developeduntil electromechanical quiescence developed
enhanced myocardial oxygen consumptionenhanced myocardial oxygen consumption
preserved highpreserved high--energy phosphate storesenergy phosphate stores
buffering changes in pHbuffering changes in pH
use of free radical scavengers (superoxideuse of free radical scavengers (superoxidedismutase, catalase, and glutathione)dismutase, catalase, and glutathione)
provide appropriate osmotic environment forprovide appropriate osmotic environment formyocardial cells and lessen the myocardialmyocardial cells and lessen the myocardialoedemaoedema
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�� Most effective at 20Most effective at 20°°C, if too cold have increasedC, if too cold have increased
blood viscosity and reduced oxygen dissociationblood viscosity and reduced oxygen dissociation
from Hbfrom Hb
�� Clinically shows little/no benefit over crystalloidClinically shows little/no benefit over crystalloid
cardioplegiacardioplegia
�� More complex & expensive than crystalloidMore complex & expensive than crystalloid
�� May show benefits for long ischaemic periodsMay show benefits for long ischaemic periods
and in poor ejection fraction patientsand in poor ejection fraction patients
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Cold Blood CardioplegiaCold Blood Cardioplegia
pitfallspitfalls hypothermic inhibition of hypothermic inhibition of
mitochondrial enzymesmitochondrial enzymes
shifting oxyhaemoglobinshifting oxyhaemoglobin
dissociation curve to leftdissociation curve to left activating platelets,activating platelets,
leukocytes, complementleukocytes, complement
impaired membraneimpaired membrane
stabilizationstabilization
advantagesadvantages
lowers myocardiallowers myocardial
oxygen demandsoxygen demands
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KCl KCl
Produce/maintain diastolic arrestProduce/maintain diastolic arrest
�� Usually 10Usually 10 -- 30 mEq/l30 mEq/l
HistidineHistidine
BufferBuffer
Mannitol Mannitol
�� Contributes to a hypertonic cardioplegiaContributes to a hypertonic cardioplegia
�� Also has free oxygen radical scavengingAlso has free oxygen radical scavenging
benefitsbenefits
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MgMg�� Potentially can induce cardiac arrest by itself Potentially can induce cardiac arrest by itself �� Stabilises cell membranesStabilises cell membranes
�� Blocks phosphorylase action of myosin therebyBlocks phosphorylase action of myosin therebypreserving high energy substratespreserving high energy substrates
�� Slow calcium channel blockerSlow calcium channel blocker
ProcaineProcaine
�� Is by itself a cardioplegic agent; blocksIs by itself a cardioplegic agent; blockspermeability of cell membrane to sodiumpermeability of cell membrane to sodiumduring repolarisationduring repolarisation
�� Slow calcium channel blockerSlow calcium channel blocker
�� Also stabilises cell membraneAlso stabilises cell membrane�� Prevents vasoconstriction due to the particlePrevents vasoconstriction due to the particlecontents of the IV solution thereby improvingcontents of the IV solution thereby improvingdistribution of cardioplegia in coronary arterydistribution of cardioplegia in coronary arterydisease; coronary vasodilatordisease; coronary vasodilator
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CalciumCalcium
�� Essential to myocardial contractility and to maintain normalEssential to myocardial contractility and to maintain normal
membrane functioningmembrane functioning
�� But implicated in reperfusion injury [But implicated in reperfusion injury [³calcium paradox´ ³calcium paradox´ ]]
�� Therefore most institution include a small amount of Therefore most institution include a small amount of
calcium in crystalloid cardioplegia (1mM/L)calcium in crystalloid cardioplegia (1mM/L)
�� Blood cardioplegia does not need any additional calciumBlood cardioplegia does not need any additional calcium
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Aspartate/GlutamateAspartate/Glutamate
metabolic substratemetabolic substrate
GlucoseGlucose
metabolic substratemetabolic substrate
BloodBlood
O2 carrying capacityO2 carrying capacity
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Cardioplegic RouteCardioplegic Route
antegrade (aorta)antegrade (aorta)
retrograde (coronary sinus)retrograde (coronary sinus)
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Antegrade CardioplegiaAntegrade Cardioplegia
pitfallspitfalls poor distribution inpoor distribution in
c oronary patientsc oronary patients unlessunless
delivered through thedelivered through thevein graftsvein grafts
poor distribution inpoor distribution inpatients withpatients with aorti c aorti c regurgitationregurgitation
risk of risk of ostial injury ostial injury fromfromdirect perfusion (duringdirect perfusion (duringAVR)AVR)
interruption of procedureinterruption of procedureduringduring mitral surgery mitral surgery
AdvantagesAdvantages
Produces promptProduces promptarrestarrest
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Retrograde CardioplegiaRetrograde Cardioplegia
perfusion pressure < 40 mmHgperfusion pressure < 40 mmHg
prevent perivascular haemorrhage andprevent perivascular haemorrhage and
oedema!oedema!
flow rate = 200mL/minflow rate = 200mL/min
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Retrograde CardioplegiaRetrograde Cardioplegia
advantagesadvantages
distribution of CP todistribution of CP to
regions supplied byregions supplied by
occluded or stenosedoccluded or stenosedvesselsvessels
improvedimproved
subendocardial CPsubendocardial CP
deliverydelivery
flushing of air and/orflushing of air and/or
atheromatous debrisatheromatous debris
pitfallspitfalls
shuntingshunting of CP intoof CP into
ventricular cavities viaventricular cavities via
Thebesian channelsThebesian channels
perfusion defectsperfusion defects
especially right ventricleespecially right ventricle
and posterior septaland posterior septal
regionsregions
(sonicated albumin(sonicated albumin
studies)studies)
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4242
Anterograde and retrograde cardioplegia oftenAnterograde and retrograde cardioplegia often
are used together.are used together.
Anterograde cardioplegia can be used to arrestAnterograde cardioplegia can be used to arrestthe myocardium with additional doses giventhe myocardium with additional doses given
retrograde with venting of aortic root. Thisretrograde with venting of aortic root. This
maximise distribution of cardioplegiamaximise distribution of cardioplegia
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4343
REPERFUSION AFTER GLOBAL MYOCARDIALREPERFUSION AFTER GLOBAL MYOCARDIAL
ISCHEMIAISCHEMIA
POST ISCHEMIA, THE MYOCARDIUM IS COMPOSED OF APOST ISCHEMIA, THE MYOCARDIUM IS COMPOSED OF A
HETEROGENOUS POPULATION OF CELLSHETEROGENOUS POPULATION OF CELLS
�� IRREVERSIBLE DAMAGEDIRREVERSIBLE DAMAGED
�� MINIMALLY DAMAGEDMINIMALLY DAMAGED
�� STUNNED MYOCARDIAL CELLSSTUNNED MYOCARDIAL CELLS
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4444
POOR MYOCARDIAL PROTECTION BEFORE AND DURINGPOOR MYOCARDIAL PROTECTION BEFORE AND DURING
CROSS CLAMPCROSS CLAMP
�� LARGE MASS OF IRREVERSIBLY DAMAGED CELLSLARGE MASS OF IRREVERSIBLY DAMAGED CELLS
LEADING USUALLY TO PATIENT DEATHLEADING USUALLY TO PATIENT DEATH
OPTIMAL PROTECTIONOPTIMAL PROTECTION
�� VIABLE MYOCARDIUM AND SURVIVAL WITH MINIMUMVIABLE MYOCARDIUM AND SURVIVAL WITH MINIMUM
INTERVENTIONSINTERVENTIONS
SUBOPTIMAL PROTECTIONSUBOPTIMAL PROTECTION
�� POPULATION OF STUNNED CELLS WHOSE FATEPOPULATION OF STUNNED CELLS WHOSE FATE
DEPENDS ON REPERFUSION MANAGEMENTDEPENDS ON REPERFUSION MANAGEMENT
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4545
ABNORMALITIES ENCOUNTERED DURINGABNORMALITIES ENCOUNTERED DURINGREPERFUSIONREPERFUSION
STRUCTURAL
MYOCARDIAL OEDEMA
PLATELET DEPOSITION
VASCULAR INJURY
VASCULAR COMPRESSION
MECHANICAL
IMPAIRED SYSTOLICAND DIASTOLIC
FUNCTION
ELECTRICAL
HETEROGENOUS ACTIVITY
INCREASED AUTOMATICITY
BIOCHEMICAL
ACIDOSIS
DECREASED OXYGEN
UTILIZATION
DECREASED H-E-P
PRODUCTION
INCREASED
CATACHOLAMINES
INCREASED CELLULAR
CALCIUM
INCREASED FREE
RADICALS
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4646
THE RESPONSE OF MYOCARDIAL CELLS TOTHE RESPONSE OF MYOCARDIAL CELLS TO
UNCONTROLLED REPERFUSION DEPENDS IN LARGE PARTUNCONTROLLED REPERFUSION DEPENDS IN LARGE PARTON THE TIMEON THE TIME--RELATED POINT ALONG THE PATHWAY TORELATED POINT ALONG THE PATHWAY TO
CELL DEATH THAT HAS BEEN REACHED DURING THECELL DEATH THAT HAS BEEN REACHED DURING THE
PERIOD OF ISCHEMIAPERIOD OF ISCHEMIA
THE CRITICAL POINT AT WHICH THETHE CRITICAL POINT AT WHICH THE µEXPLOSIVE µEXPLOSIVE
CELLULAR RESPONSE¶ CELLULAR RESPONSE¶ TO UNCONTROLLED PERFUSION ISTO UNCONTROLLED PERFUSION IS
SEEN CANNOT BE DEFINEDSEEN CANNOT BE DEFINED
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4747
MYOCARDIAL RESPONSE TO REPERFUSIONMYOCARDIAL RESPONSE TO REPERFUSION
MYOCARDIAL STUNNINGMYOCARDIAL STUNNING
REPERFUSION ARRHYTHMIASREPERFUSION ARRHYTHMIAS
�� VENTRICULAR TACHYCARDIAVENTRICULAR TACHYCARDIA
�� VENTRICULAR FIBRILLATIONVENTRICULAR FIBRILLATION
STONE HEARTSTONE HEART
�� HARD AND FIBRILLATING HEARTHARD AND FIBRILLATING HEART
�� MAY INVOLVE ONLY SOME REGIONS OF THE HEART,MAY INVOLVE ONLY SOME REGIONS OF THE HEART,
TYPICALLY THE BASILAR PORTION OF THE LEFTTYPICALLY THE BASILAR PORTION OF THE LEFT
VENTRICLE AND THE SUBENDOCARDIUMVENTRICLE AND THE SUBENDOCARDIUM
�� INDICATES USUALLY THAT THE HEART HAS REACHEDINDICATES USUALLY THAT THE HEART HAS REACHED
THE POINT OF µNOTHE POINT OF µNO--RETURN¶, THOUGH NOTRETURN¶, THOUGH NOT
NECESSARILY SO.NECESSARILY SO.
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4848
ENDOTHELIAL CELL DAMAGE DUE TOENDOTHELIAL CELL DAMAGE DUE TO
REPERFUSIONREPERFUSION
SWELLING OF ENDOTHELIAL CELLS, AGGREGATION OFSWELLING OF ENDOTHELIAL CELLS, AGGREGATION OF
NEUTROPHILS AND PLATELET PLUGS CAUSENEUTROPHILS AND PLATELET PLUGS CAUSE
MICROVASCULAR OBSTRUCTIONMICROVASCULAR OBSTRUCTION
ADDITIONALLY, MYOCARDIAL OEDEMA CAN ALSOADDITIONALLY, MYOCARDIAL OEDEMA CAN ALSO
COMPRESS THE MICROVASCULATURE LEADING TOCOMPRESS THE MICROVASCULATURE LEADING TO
INHOMOGENEOUS REPERFUSION, OR SOMETIMES, THEINHOMOGENEOUS REPERFUSION, OR SOMETIMES, THE
µNOµNO--REFLOW¶ PHENOMENONREFLOW¶ PHENOMENON
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4949
MOLECULAR BASIS OF REPERFUSIONMOLECULAR BASIS OF REPERFUSION
RESPONSERESPONSE
INFLUX OF CALCIUM INTO MYOCYTES, ESPECIALLYINFLUX OF CALCIUM INTO MYOCYTES, ESPECIALLY
ACCUMULATION IN MITOCHONDRIAACCUMULATION IN MITOCHONDRIA
RELEASE OF COMPLEMENT FRAGMENTS SUCH AS C5a FROMRELEASE OF COMPLEMENT FRAGMENTS SUCH AS C5a FROM
ISCHEMIC MYOCARDIUMISCHEMIC MYOCARDIUM
�� CHEMOTACTIC FOR NEUTROPHILS, WHICHCHEMOTACTIC FOR NEUTROPHILS, WHICH
PLUG MYOCARDIAL CAPILLARIESPLUG MYOCARDIAL CAPILLARIES
RELEASE LARGE AMOUNT OF OXYGEN DERIVED FREERELEASE LARGE AMOUNT OF OXYGEN DERIVED FREE
RADICALSRADICALS
RELEASE ARACHIDONIC ACID METABOLITES WHICHRELEASE ARACHIDONIC ACID METABOLITES WHICH
CAUSE ENDOTHELIAL INJURY, PLATELET AGGREGATIONCAUSE ENDOTHELIAL INJURY, PLATELET AGGREGATION
AND VASOCONSTRICTIONAND VASOCONSTRICTION
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5050
FreeFree--radical Reperfusion Injuryradical Reperfusion Injury
characterised by abnormal myocardial oxidativecharacterised by abnormal myocardial oxidative
metabolismmetabolism
mediated by the interaction of cytomediated by the interaction of cyto--toxic oxygentoxic oxygen
free radicals, endothelial factors, and neutrophilsfree radicals, endothelial factors, and neutrophils
oxidising sarcolemmal phospholipids, andoxidising sarcolemmal phospholipids, and
disrupting membrane integrity (lipiddisrupting membrane integrity (lipid
peroxidation)peroxidation)
delayed myocardial metabolic recoverydelayed myocardial metabolic recovery
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5151
TherapiesTherapies
PhysiologicalPhysiological
�� superoxide dismutasesuperoxide dismutase
�� catalasecatalase
�� nitric oxidenitric oxide
PharmacologicalPharmacological
�� mannitolmannitol
�� allopurinolallopurinol
�� antioxidantsantioxidants
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5252
CONTROLLED REPERFUSIONCONTROLLED REPERFUSION
MINIMIZES THE PERSISTENCE OF MYOCARDIAL STUNNINGMINIMIZES THE PERSISTENCE OF MYOCARDIAL STUNNING
INTO THE POSTINTO THE POST--CPB PERIODCPB PERIOD
PROVIDES FOR OPTIMAL RECOVERY OF FUNCTION OFPROVIDES FOR OPTIMAL RECOVERY OF FUNCTION OF
REVERSIBLY DAMAGED MYOCARDIUMREVERSIBLY DAMAGED MYOCARDIUM
RESUSCITATES MYOCYTES THAT WOULD OTHERWISERESUSCITATES MYOCYTES THAT WOULD OTHERWISE
HAVE UNDERGONE NECROSISHAVE UNDERGONE NECROSIS
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5353
CONTROLLED REPERFUSION CONSISTS OF THECONTROLLED REPERFUSION CONSISTS OF THE
FOLLOWING:FOLLOWING:
MAINTINING ELECTROMECHANICAL QUIESCENCE DURING THEMAINTINING ELECTROMECHANICAL QUIESCENCE DURING THE
FIRST 3FIRST 3 ±± 5 MINS. OF REPERFUSION5 MINS. OF REPERFUSION
�� PERMITS MORE RAPID REPLETION OF MYOCARDIAL ENERGYPERMITS MORE RAPID REPLETION OF MYOCARDIAL ENERGY
CHARGECHARGE
�� MINIMIZES REGIONAL HETEROGENECITY OF FLOWMINIMIZES REGIONAL HETEROGENECITY OF FLOW
�� MINIMIZES MYOCARDIAL ENERGY EXPENDITURE TILLMINIMIZES MYOCARDIAL ENERGY EXPENDITURE TILL
RECOVERY HAS BEEN ESTABLISHEDRECOVERY HAS BEEN ESTABLISHED
�� MINIMIZES INTRACELLULAR ACCUMULATION OF CALCIUMMINIMIZES INTRACELLULAR ACCUMULATION OF CALCIUM
LARGE BUFFERING CAPACITY OF REPERFUSATE TO COMBATLARGE BUFFERING CAPACITY OF REPERFUSATE TO COMBAT
ACCUMULATED ACIDOSISACCUMULATED ACIDOSIS
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5454
MINIMIZING DAMAGE BY OXYGENMINIMIZING DAMAGE BY OXYGEN--DERIVED FREEDERIVED FREE
RADICALSRADICALS
MAINTAINING LOW CALCIUM IN THE INITIAL PERFUSATEMAINTAINING LOW CALCIUM IN THE INITIAL PERFUSATE
TO PREVENT INTRACELLULAR ACCUMULATION OF CALCIUMTO PREVENT INTRACELLULAR ACCUMULATION OF CALCIUM
SUBTRATE ENHANCEMENT OF THE REPERFUSATE FORSUBTRATE ENHANCEMENT OF THE REPERFUSATE FOR
REPLETION OF ENERGY CHARGEREPLETION OF ENERGY CHARGE
MAINTAINING LOW PERFUSION PRESSURES AROUND 30MAINTAINING LOW PERFUSION PRESSURES AROUND 30 ±±
40 mmHg DURING THE FIRST COUPLE OF MINUTES OF40 mmHg DURING THE FIRST COUPLE OF MINUTES OF
REPERFUSION TO MINIMIZE ENDOTHELIAL CELL DAMAGEREPERFUSION TO MINIMIZE ENDOTHELIAL CELL DAMAGE
AND SWELLINGAND SWELLING
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5555
SUGGESTED STRATEGIES FOR CONTROLLEDSUGGESTED STRATEGIES FOR CONTROLLED
REPERFUSIONREPERFUSION
USING BLOOD AS THE REPERFUSATE INSTEAD OFUSING BLOOD AS THE REPERFUSATE INSTEAD OF
CRYSTALLOIDCRYSTALLOID
�� RBCs CONTAIN ABUNDANT FREE RADICAL SCAVENGERSRBCs CONTAIN ABUNDANT FREE RADICAL SCAVENGERS
�� BUFFERING CAPACITY OF BLOOD PROTEINSBUFFERING CAPACITY OF BLOOD PROTEINS
SUBSTRATE ENHANCEMENT s/a GLUTAMATE OR LSUBSTRATE ENHANCEMENT s/a GLUTAMATE OR L--
ASPARTATEASPARTATE
BUFFERING AGENTS SUCH AS HYDROXYMETHYALBUFFERING AGENTS SUCH AS HYDROXYMETHYAL
AMINOMETHANE AND HISTIDINEAMINOMETHANE AND HISTIDINE
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5656
ENOUGH POTASSIUM CONTENT TO MAINTAINENOUGH POTASSIUM CONTENT TO MAINTAIN
ELECTROMECHANICAL QUIESCENCE, USUALLY 10ELECTROMECHANICAL QUIESCENCE, USUALLY 10 ±± 2020
mEq/LmEq/L
OPTIMUM PERFUSION PRESSURE OF THE REPERFUSATEOPTIMUM PERFUSION PRESSURE OF THE REPERFUSATE
MAINTAINING TEMPERATURE OF REPERFUSATE BETWEENMAINTAINING TEMPERATURE OF REPERFUSATE BETWEEN
3535 ±± 37 DEG. CENT.37 DEG. CENT.
CONTINUING CONTROLLED REPERFUSION TILL THE HEARTCONTINUING CONTROLLED REPERFUSION TILL THE HEART
IS BEATING FORCEFULLY, PREFERABLY IN SINUS RHYTHMIS BEATING FORCEFULLY, PREFERABLY IN SINUS RHYTHM
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