intraoperative myocardial protection

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1 Intraoperative Intraoperative Myocardial Protection Myocardial Protection PRESENTOR PRESENTOR ± ± Dr. Sameer goyal Dr. Sameer goyal MODERATOR MODERATOR ± Dr . S.K. Mathur  Dr. S.K. Mathur Dr. R.K Dubey Dr. R.K Dubey 

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8/7/2019 Intraoperative Myocardial Protection

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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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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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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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TherapiesTherapies

PhysiologicalPhysiological

�� superoxide dismutasesuperoxide dismutase

�� catalasecatalase

�� nitric oxidenitric oxide

PharmacologicalPharmacological

�� mannitolmannitol

�� allopurinolallopurinol

�� antioxidantsantioxidants

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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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5757

Thank you!Thank you!