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ANAESTHETIC
CONSIDERATIONS IN
CPB
BY- DR SUCHIT
KHANDUJA
MODERATOR-PROF
SURINDER SINGH
DEFINITION
• “CPB is the technique whereby blood is
totally or partially diverted from
the heart into a machine with the gas
exchange capacity and subsequently
returned to the arterial circulation at
appropriate pressures & flow rates.”
HISTORICAL ASPECTS
• Legllois (1812) : “circulation
might be
taken over for short periods”
• Dr.John Gibbon(Philadelphia) 1953 :
“performed ASD repair with the aid of
CPB for the 1st time with the survival of
patient.”
GOALS OF CPB
• To provide a still &
Bloodless Heart with
blood flow temporarily
diverted to an
Extracorporeal Circuit
that functionally replaces
the Heart & the Lung
GOALS OF CPB
RESPIRATION
Ventillation
Oxygenation
CIRCULATION
TEMP. REGULATION (Hypothermia)
Low blood flowso ed blood trauma
ses Body Metabolism.
COMPONENTS OF CPB
• TOTAL CPB : Systemic venous drainage
CPB Circuit  External oxygenator heat
exchanger External pump arterial
filterSystemic circulation.
• PARTIAL CPB : Portion of systemic
venous return (Rt. Heart)  CPB .Undiverted
blood  Rt. Atrium  Rt. Ventricle  Pul.
Circulation  Lt. Atrium & Lt. Ventricle 
Systemic Circulation.
INTEGRAL COMPONENTS OF extracorporeal
circuit
• PUMPS
OXYGENATOR
Heat exchanger
Arterial filter
Cardioplegia delivery system
Aortic/atrial/vena caval
cannulae
Suction/vent
PATIENT
ARTERIAL
LINE
FILTER
RESERVOIR
ROLLER
PUMP
OXYGENATOR
HEAT
EXCHANGER
ROLLER PUMP
• Most commonly used.
• Uses Volume displacement to create
forward blood flow.
• Non Pulsatile Blood Flow
• By compressing Plastic Tubing b/w Roller &
Backing Plate
• Properly set occlusion causes minimal
haemolysis
• Occlusion is 100% in cardioplegia &vent pumps
• Each pump indepedently controlled by a rheostat
• Larger tubing and lesser rotations cause minimal
haemolysis
• Resistance= resistance of
tubing+oxygenator+heat
excyhanger+filter+aortic cannulae+SVR
• Usually line pr. depends on SVR and pump
flow rate
• Nl limit is 150-350 mm hg( >250 is seldom
accepted)
DISADVANTAGE of producing PULSATILE
FLOW
Bubble Formation
Damage to Blood Components.
ADVANTAGE :
 Improved Tissue Perfusion
 Better Preservation of Organ Function (Brain , Kidney)
CENTRIFUGAL PUMP
• Series of CONES that spin & propel blood
forward by Centrifugal Force.
• Safe
• Reliable
• Disposable
• Simple to operate.
CENTRIFUGAL PUMP
• ADVANTAGE
 No back pressure when tubing
is temporarily obstructed /
kinked
 Doesn’t produce spatulated
emboli from compression of
the tubing
 Cannot pump large amt.of gas /
gas emboli.
 Less blood trauma
 High vol. output with moderate
pressures
• DISADVANTAGE
Inability to generate
pulsatile flow
Potential discrepancy b/w
pump speed & actual flow
generated.
• Preferred over roller pumps in
• Long-term CPB
• In high-risk angioplasty patients
• Ventricular assistance
• Neonatal ECMO
• Pressure-regulated pump
• Operates under passive filling
• After&pre-load sensitive
• Pump-chamberof polyurethane+peristaltic
pump
• Not yet fully evaluated
OXYGENATOR
• Where O2 & CO2 Exchange takes place.
• Two Types :
BUBBLE OXYGENATOR
MEMBRANOUS OXYGENATOR
BUBBLE OXYGENATOR
• Gas exchange by directly infusing the gas into a
column of systemic venous blood.
• A) OXYGENATING CHAMBERS : bubbles produced
by ventilating gas through diffusion plate into venous blood column
• CO2  bubble & oxygen  plasma
• Larger the No. of Bubbles ; Greater the efficiency of the oxygenator.
• Larger bubbles improve removal of CO2 , diffuses 25 times more rapidly in
plasma than O2
•
Smaller bubbles are very efficient at oxygenation but poor in co2 removal
DEFOAMING CHAMBER
• Defoaming of frothy blood.
• Large surface area coated with silicone
• This es the Surface Tension of the bubbles
causing them to burst.
BUBBLE OXYGENATOR
•
•
•
•
ADVANTAGE
Easy to assemble
Relatively small
priming Volumes
Adequate oxygenating
capacity
Lower cost.
•
•
•
•
•
DISADVANTAGE
Micro emboli
Blood cell trauma
Destruction of plasma
protein due to gas
interface.
Excessive removal of
CO2
Defoaming capacity
may get exhausted
with time.
MEMBRANOUS OXYGENATOR
• Gas exchange across a thin membrane
• Eliminates the need for a bubble-blood contact
& need for a defoamer; so more physiological.
• Blood damage is minimum
• Ideal for perfusions lasting for >2-3 hours.
• 2 types of membrane:
• SOLID: Silicone
• MICROPOROUS: polypropylene,Teflon
&polyacrylamide
MEMBRANOUS OXYGENATOR
ADVANTAGE
• Can deliver Air-O2
mixtures.
• Hemolysis
•  Protein
desaturation
•  Post-op bleeding
• Better platelet
preservation.
DISADVANTAGE
• Expensive
• Large priming
volume
• Prolonged use
pores may get
blocked.
CIRCUITS
† Drains Venous Blood by gravity into
oxygenator & returns the oxygenated
blood under pressure to the systemic
circulation.
VENOUS DRAINAGE
• Systemic venous blood
(Rt.Heart)Oxygenator by
Direct Cannulation of SVC & IVC (Bicaval
Cannulation) thru RA & joined to create a
single drainage channel.
Single cannula into RA thru RA appendage.
• Blood flow Oxygenator (Gravity)
• Height Difference B/w Venacavae &
Oxygenator > 20-30 cm.
Complications
• arrhythmia
• bleeding
• ivc/svc tear
• cannula malposition
• low return
• inadequate height
• malposition
• kink,clamp,air lock
Size of cannula
Adults
Children
SVC
28G
24G
IVC
36G
28G
TUBINGS IN THE CIRCUIT
• Non thrombogenic , Chemically Inert to prevent
clotting
Trauma to blood elements
Protein Denaturation
• Smooth Internal Finish
• Non Reactable Internal Surface
• Durable to withstand high pressure & use of Roller
pump
• Made of
• PVC
• Polyurethane
• Silicone
• I.D . Ranges from 3/16- 5/8 inches
• HEPARIN BONDED CIRCUITS ARE AVAILABLE
Disadvantages of plain circuits
• Activation of platelets/coagulation factors
• Post-op consumptive coagulopathyimmune
reactions
• More spallation
Heparin coated circuits are
• More hemo compatible
• Cause less activation of platelets/white cells
• Reduce heparin demand
INTRACARDIAC SUCTION
• Blood will enter the heart
Coronary venous Return
Retrograde flow in AR.
Bronchial Arteries
 CARDIOTOMY SUCTION
• Spilled Heparinised Blood is Scavenged &
returned back to patient.
• Handheld Suckers are used to return this
blood.
VENTRICULAR VENTING
• LV Venting done to
• Keep the operative field clear
• Maintain Low LA & Pul.Venous Pressure
• Remove air from Cardiac Chamber.
•Blood from LV  Reservoir Bag
RESERVOIR BAG
• Collects the blood from VENOUS DRAINAGE &
CARDIOTOMY SUCTION DRAIN PASSIVELY
Reservoir Bag  Oxygenator Heat exchanger 
Arterial Filter  Patient.
• Volume in the bag should not be allowed to empty
to prevent massive emboli.
ARTERIAL RETURN
• Ascending Aorta just proximal to Innominate Artery.
• Femoral Artery in
Dissecting Aortic Aneurysm
For Reoperation
Emergency
• Problems of Femoral Cannulation :
• Sepsis
• Formation of False Aneurysm
• Development of Lymphatic Fistula.
ARTERIAL CANNULA
• Is the Narrowest part of the circuit.
• Should be as Short as possible.
• As Large as the diameter of vessel permits.
Complications
• Difficult Cannulation
• Intramural Placement
• Air embolism
• Dislodgement of Cannula
• Dissection
• Arch Vessel Cannulation
• Back Wall Injury
• MICROPORE FILTERS:
• Remove Particulate Matter (Bone , Tissue , Fat
, Blood Clots etc.)
• Pore Size : 30 – 40 
• ULTRAFILTRATION :
• Remove the excess fluid from the CPB.
PRIME FLUID
• Ideally close to ECF.
• Whole Blood NOT used :
• Homologous Blood Syndrome.
• Post Perfusion Bleeding Diathesis
• Incompatibility Reactions.
• Demand on Blood Banks.
• Addition of Priming Fluid  HEMODILUTION.
COMPOSITION OF PRIME :
• Balanced salt soln. RL
• Osmotically active agent
(Mannitol, Dextran 40 , Hexastarch)
• NaHCO3
• KCl
• Heparin
1250 ml
100 ml
50ml
10ml
1ml
PRIMING
• Heme, nonheme
• Decreases viscosity so better flow
• Attenuates increased viscosity by hypothermia
• Alters pharmacodynamics and kinetics of drugs
• Decreases Hb but improves O2 delivery
• Lowest acceptable value 8g/dl
• Prediction of initial haematocrit during CPB
Predicted Hct
=
volume
– EBV
• Infants
• Children
• Adult (male)
• Adult (female)
Pt. RBC volume before CPB
/ Pt. EBV + CPB prime
80-85 ml/kg
75ml/kg
70ml/kg
65ml/kg
– 1U packed cells = 0.7 x 350 = 245ml
– IU whole blood = 0.4 x 350 = 140ml
• Amount of priming fluid
• CVX CPCV = Pt. BV X PCV + PV X PCV
• PT.BLOOD VOL. x PT. HEMATOCRIT = TARGET
HCT X(PRIME VOL. + PT. BLOOD VOL.)
PATHOPHYSIOLOGY OF CPB
• THREE MAJOR PHYSIOLOGICAL ABERRTIONS
ARE:
1.LOSS OF PULSATILE FLOW
2.EXPOSURE OF BLOOD TO NON-PHYSIOLOGIC
SURFACES & SHEAR STRESSES.
3.EXAGGERATED STRESS RESPONSE.
CIRCULATORY SYSTEM
•
SVR : Initial Phase SVR 
i.
 Blood Viscosity 20 to Hemodilution.
ii.
Vascular Tone d/t dilution of circulatory catecholamines
As CPB  BP  , d/t  SVR
a)
Actual  in Vascular C/S area d/t closure of portions of
microvasculature.
b)
 Catecholamines
c)
VC d/t hypothermia.
• Cardiac output : flow rate at 2.2-2.4 l/m2/min at 370c.
• BP : 0-70 mm Hg.
• Venous tone : Close to zero
PULMONARY EFFECT
• Activated neutrophils (elastase &lysosomal
enzyme ) accumulate within the lungs
during CPB.
• Pul. Venous Pressure , 20 to LAP ,
es the risk of Pul.Interstitial Edema.
* After CPB Pul.Compliance falls & Airway
Resistance  leading to Work of
Breathing.
CNS CHANGES
• Embolic phenomena :
–Air
–Preexisting thrombi
–Platelet & leucocyte aggregate
–Fat globules
• Hemodilution –> mild cerebral edema
• CBF when MAP es <40mmHg during CPB
RENAL EFFECT
• MICRO EMBOLI
• Vasoconstrictors
• Ppt. of Plasma Hb in Renal tubules U.O.
• Long term ace inhibitor therapy can result in
decline in glomerular filteration pressure
HEMATOLOGIC EFFECT
• RBC : become stiffer & less distensible
–Exposed to Non-physiologic surfaces
– Hemolysis d/t high flow rates
• WBC : Marked  in PMN
• PLATELETS : aggregation & dysfunction
thrombocytopenia.
HEMATOLOGIC EFFECT
• PLASMA PROTEIN :Denaturation 
– Altered enzymatic function
– Aggregation of platelets
– Altered solubility characteristics
– Release of lipids
– Absorption of denatured proteins into cell
membranes.
NEUROENDOCRINE RESPONSE TO CPB:
• Serum Catecholamines : 
–Both ADR & NA 
–D/t reflexes from Baroreceptors &
Chemoreceptors in the Heart & Lungs
when the organs are excluded from
circulation.
• ADH,Cortisol , Glucagons & GH are 
INDUCTION OF ANAESTHESIA
• Choice depends on haemodynamic status
1. High dose opioid anesthesia
2. Total intravenous anesthesia
3. Mixed iv/inhalational agent anesthesia
• High dose opioid
• Fentanyl -50-100mic/kg,sufentanil 15-25mic/kg
ADV-Faster extubation
Disadvantage1. Prolonged respiratory depression
2. Chest wall ridgidity
3. Patient awareness
4. Inability to control hypertensive response
Total iv anaesthesia
• Propofol 1-2 mg/kg with infusion of 50100mic/kg/min
• Remifentanil 0-1mic/kg bolus followed by .251mic/kg/min
• TCI may be used
Mixed IC/Inhalational anesthesia
• Interest grew after studies on protective effect of
volatile agents on myocardium
• Propofol,thiopentone,midazolam may all be given
• Opioid given in smaller dosages with inhalational
agent at .5-1.5 MAC
• Isoflurane,sevoflurane and desflurane used
• N2O not used because of its tendency to expand
bubbles in intravasular compartment during CPB
• Isoflorane.desflorane and sevoflorane cause
dose dependent vasodilation.
• Also lead to ischaemic preconditioning.
• N20 usually avoided .
• Radial artery is cannulated.
• Contralateral femoral also used as conduit.
• Cvp catheter or PA catheter or both
introduced.
• Bladder catheter,temp. probe and TEE probe
positioned.
PRE-CPB
Two stages
– High level of stimulation
• Skin incision, sternal split, sternal spread, aortic
dissection cannulation.
• Increase HR, BP, ischemia, dysrhythmias, HF
– Low level of stimulation
• Preincision, Radial artery harvesting,
dissection, CPB venous cannulation.
• Decrease HR, BP, ischemia, dysrhythmias
LIMA
•
•
•
•
•
All injection ports should be accessible
Monitoring lines should be well secured
Confirm zero of all transducers
Evaluate cardiac status by TEE (placed before heparin).
Once patient stabilized
– ABG, ACT, BSL, Serum electrolytes
• Antibiotics
• Antifibrinolytics
– Aprotinin, EACA, Transexamic acid
• Pre-incision, sternal split
–
Supplemental - Narcotics, relaxants, hypnotics, inhaled agents.
–
Ensure adequate depth of anaesthesia.
• Redo case
–
Lateral CXR provides a clue to potential problems
–
Longer time required than routine
–
Femoral vessels to be prepared
–
External defibrillator
–
Adequate volume replacement – crystalloids, colloids, blood and
blood products.
HEPARIN
• Jay Mclean-1916, William Howell
• N-sulfated-D-Glucosamine& L-iduronic acid
• strongest acid, anionic, negative charged
• Heterogenous compound, mol wt 5000 – 30000 (most chains
12000-19000).
• UFH dose should not be specified by weight but by units.
• 1 USP of heparin activity is the quantity that prevents 1 ml of
citrated sheep”s plasma from clotting for 1 hr after addition of
calcium.
• Standard heparin is UNFRACTIONATED HEPARIN (UFH ).
• Heparan
• found in CT, contains more of glucuronic acid >20% Nacetylation.
• Abundant in tissues rich in mast cells
• liver, lungs, intestines
• skin, lymph nodes, thymus lesser sources.
• Two sources
• Bovine lung
• Porcine intestinal mucosal ( most commercial prep ,
40000 lbs yield 5kg heparin)
• Pharmacokinetics & dynamics:
•
3 compartment model describes heparin kinetics
•
Rapid initial clearance from endothelial cell uptake
•
Saturable clearance seen in lower doses due to uptake by RES & its
endoglycosidases, endosulfatases & uptake into monocytes.
•
Exponential decay seen at higher doses due to renal clearance via tubular
secretion.
• Metabolism:
•
50%- RES
•
50%- Renal elimination
• Actions:
•
Exerts its actions via AT-III which inhibits thrombin, IXa, Xa.
•
UFH accelerates the formation of thrombin-AT complex 2000 X, Xa-AT
complex 1200X
•
LMWH preferentially inhibits Xa
HEPARIN RESISTANCE/ ALTERED HEPARIN RESPONSIVENESS:
• Pts previously receiving heparin exhibit tachyphylaxis,
diminished response to full anticoag doses of UFH for CPB.
Risk Factors:
• Elderly/ neonates
•
IABP
• Previous heparin therapy
•
Shock
• OCP/ Pregnancy
•
STK
• Thrombocytosis
•
Infective endocarditis
• Congenital AT-III deficiency
•
Ventricular aneurysm with
thrombus
•
Consumptive coagulopathy
• Hemodilution
• Dose:
• 3-4 mg/ kg
• 300-400 u/ kg
• given in central vein or directly into RA
• use HDR
• always confirm with ACT
 UFH chelates Ca, large bolus- decline in BP due to
decrease in SVR & preload.
 Immunologic effects-30-50% pts of cardiac surgery have
heparin Abs by the time of hospital discharge
• Arterial sample in 3-5 min
• Give additional heparin as needed to maintain
ACT >300 s in normothermic and >400 s in
hypothermic CPB
• Monitor ACT every 30 min or more frequently
if pt.is heparin resistant
• If ACT goes <300 s give additional 50 u/kg
heparin
ACTs
• <180 s - life threatening
• 180-300 s -highly questionable
• >600 s –risky and unwise
• Individual anticoag response to heparin varies , hence
measurement of individual anticoag response to heparin for CPB is
warranted. Usually heparin effect is measured and not its plasma
levels.
TREATMENT
– Additional heparin
– AT-III concentrate (1000 u increases AT-III levels by 30%
– rhAT trials on (75 U/ kg)
– FFP ( risk of infection transmission, reserved for rare
refractory cases)
HEPARIN REBOUND
• pts develop clinical bleeding assoc with prolongation
of coagulation times due to reappearance of
circulating heparin.
CAUSES
– late release of heparin sequestered in tissues
– delayed return of heparin to circulation from extracellular
space via lymphatics
– clearance of
antagonist
an
unrecognized
endothelial
– more rapid clearance of protamine to heparin.
• Incidence-50%
• Can occur as soon as 1 hr after prota adm
heparin
TREATMENT:
• Clinical bleeding does not always accompany heparin
rebound.
• If + -additional supplemental protamine.
• Larger initial doses may decrease likelihood but risk of
adverse cardiovasc sequelae & anticoag effects of
protamine.
• Use HDR to calculate heparin.
HIT
• Heparin normally binds to platelet memb at GP Ib and
aggregates normal platelets by releasing ADP.
• Type-I
– moderately reversible
– Prolongation of BT
• Type-II
– Occ severe & progressive thrombocytopenia (<1 lac)
– Accom by severe fatal thrombosis
– Drop in platelet count > 30-50% over several days in a pt receiving or
finished receiving heparin.
• Heparin dependent Abs usually IgG present, lower titres
during therapy but rise once therapy ceases.
DIAGNOSIS:
• Incidence 1-3%
• Dose related but can occur even with heparin flush or
heparin bonded intravascular catheters.
• Usually 3-15 days after heparin but can occur within
hours in a pt previously exposed to heparin
• Decrease in platelet counts
• Serotonin release assay- pt plasma + donor platelets
containing radiolabelled serotonin + heparin.
• ELISA for Ab to hep-PF4 complex.
Treatment
• PC not indicated
• Discontinue heparin
• Start alternative anticoag
• Surgery for thrombosis
• Aspirin, ticlopidine, dipyridamole block adhesion and activation
and PF4 release
• Delay surgery to wait for Abs to regress
• Plasmapheresis
• Heparin substitutes
HEPARIN SUBSTITUTES
CANNULATION
• Aortic cannula first
– Maintain SBP to 90-100
– MAP 60 –80
– Excessive lowering – damage to posterior wall
– Largest possible size
• Check line pressures
• Sandblasting effect
• Coanda effect
Complications
• Difficult Cannulation
• Intramural Placement
• Air embolism
• Dislodgement of Cannula
• Dissection
• Arch Vessel Cannulation
• Back Wall Injury
• Venous Cannulation
– Single stage
• Atrial
• Bicaval
– Two stage
• Atriocaval
– Peripheral
• size is important
Complications
• arrhythmia
• bleeding
• ivc/svc tear
• cannula malposition
• low return
• inadequate height
• malposition
• kink,clamp,air lock
HYPOTHERMIA
•
•
•
•
Decreases BMR VO2, VCO2
Provides organ protection and safety margin
Decreases excitatory NT (glutamate) release
Decreases rate of enzymatic reaction
• Q10 - change in reaction rate for 100C (2-3)
• Can use non sanguinous primes and lower flows
• Increases SVR, PVR
• Decreases blood trauma
• Decreases blood flow to all tissues but also req.
• Decreases HR
• Dysrhythmia occur
– Nodal, VPC, AF, VF, blocks, asystole
• Decreases ventilation
• Left ward shift of ODC
• Increases dead space – no effect on gas exchange
• Increases renal vascular resistance
• Decreases renal blood flow
• Decreases tubular reabsorption
• Urine flow may be increased
• Hepatic blood flow decreased
• Decreased metabolic and excretory liver function
• Marked hyperglycemia – decrease insulin increased
catechol
• Affects coagulation by platelet dysfunction and
inhibition of coagulation factor.
Mild
32 –350C
Moderate
-
Deep
18-260C
Profound
-
26-310C
<180C
• Cooling / rewarming facilitated by increasing pump
flow rates and dilators.
• Gradient < 5-100C, never exceed 400C.
NORMOTHERMIC CPB
• Warm cardioplegia
– Better myo substrate use
– (L) ODC shift avoided
– Diastolic arrest produces greatest reduction in
MVO2
– Continuous CP attenuates reperfusion injury
• No need for rewarming
• Earlier extubation
• Lower SVR so higher flow rates, vasoconstrictors
Ideal temperature – indeterminate
• Tepid CPB
32-340C
• Terminate CPB 34-350C
MEAN ARTERIAL PRESSURE
• maintain 70-90 @ normothermia
• 50-70 mm Hg 30-32°C
• 30-40 mm Hg @ <30°C
• Higher pressures- increased non coronary collateral
flow
• Maintain adequate flows
• SVR– increased by phenylephrine, noradr
– decreased by NTG, SNP, anaesthetics
Sub-groups needing higher pressure
• Severe atherosclerosis
• Advanced age
• Hypertension
• Diabetes
CPB INFLAMMATORY RESPONSE
• Blood contact with non endothelial surface
• Complement system, monocyte- macrophage
system, cytokines, endotoxins, free
radicals,metalloproteinases
• Systemic inflammatory response to bypass
MONITORING
PATIENT
• ECG
• CVP/ PAC
• Arterial/ Perfusion pr
• Temperature
• Coagulation-ACT,TEG
• Urine output
• SpO2 ,EtCO2
• Se electrolytes
• ABG
• Hb, Hct
• BSL
• TEE
• EEG, BIS
• SjvO2
PUMP
Inline blood gas monitoring
Venous oximetry
Line pressure
Temperature monitoring
Flow
Reservoir volume
Bubbles
CARDIOPLEGIA
Route
• antegrade
 aortic root, ostial
 maintain root pressure 50-100 mm Hg
• retrograde
 coronary sinus
 maintain coronary sinus pressure 40-60 mm Hg
Temp
• warm
• tepid
• cold
Interval
• continuous
Vehicle
• blood
• crystalloid
•
•
•
•
total dose is 20-30 ml/ kg
target myocardial temp. is 10-15ºC
repeat every 20-30 min
dose is usually ½ the induction dose with ½ the
potassium conc. of the induction soln.
AIMS OF CARDIOPLEGIC ARREST
• induce arrest as quickly as possible
• provide oxygenation
• maintaining cellular integrity by maintaining Na-K ATPase
• provide energy substrates for metabolism
• maintain osmolarity to prevent cellular edema
• possess buffering capability,oxygen free-radical scavenging capacity (best
by blood )
• hypothermia helps in decreasing oxygen demand
ULTRAFILTRATION
• hydrostatic pressure
• increased by increasing perfusion pressures or by
applying vacuum on the effluent side of the memb
• pore size is imp (10-35 A°) (20000 Da)
• Alb, Hb, fibrinogen, blood cells remain back
• MUF
– after separation from CPB
– blood from aortic cannula thru hemoconc to RA
• CUF
– performed during rewarming
– volume removed is based on volume in CPB circuit
– Limited in pediatric pt. (<10kg,small intravasc vol)
& stopped once CPB is off
• High Volume Zero UF
– modification of CUF
– UF volume is replaced with equal volume of
crystalloid
Advantages:
• removal of free water
• preservation of hemostasis
• increases Hb,plat counts, fibrinogen, albumen
• removes proinflammatory mediators-complements,
TNF, IL-1, IL-6,IL-8
• removal of C-3a-decreases PVR, improves
oxygenation, faster extubation
• improves post-CPB hemodynamics- lower HR, inc
SBP, higher cardiac index, better diastolic compliance
• decreases cerebral edema
• improves renal function post CPB
WEANING FROM CPB
C
V
P
Cold
Ventilation
Predictor
Conduction
Visualisation
Pressure
Cardiac output
Vapourizer
Pressors
Cells
Volume expander
Pacer
Calcium
Potassium
Coagulation
Protamine
PROTAMINE
•
•
•
•
•
•
Meischer 1868, Hagedorn & colleagues 1936
contains many positive charges, nearly 2/3rd arginine
Chargaff & Olson- neutralizing drug
salmon milt
Stable without refrigeration for several weeks
Available as sulfate & chloride salts ( Chloride has more
rapid onset of action)
Actions:
• Formation of complexes with sulfate groups of heparin
form the basis for antidote effect
• Neutralizes AT effect of heparin far better than anti Xa
effect, hence poor ability to neutralize LMWHs
Advantages:
•
•
•
•
•
•
•
•
removal of free water
preservation of hemostasis
increases Hb,plat counts, fibrinogen, albumen
removes proinflammatory mediators-complements,
TNF, IL-1, IL-6,IL-8
removal of C-3a-decreases PVR, improves
oxygenation, faster extubation
improves post-CPB hemodynamics- lower HR, inc
SBP, higher cardiac index, better diastolic compliance
decreases cerebral edema
improves renal function post CPB
• Recommended doses to neutralize heparin vary
widely
• lot of controversy regarding optimal prota-hep ratio,
dose to prevent rebound & whether to calculate
prota dose based on total amt of hep given or amt
remaining in the pt.
• Normally 1.3-1.5 X heparin doses, 75% given foll CPB
& 25% foll reinfusion of pump blood
• Best to use protamine titration tests
GUIDELINES FOR USE:
• Add to 50 ml clear infusion & adm infusion over 10-15min
• Additional doses of undiluted prota given @20mg/ min
• Slow adm decreases Type I & Type III adverse reactions but Type II can
occur at any delivery rate
• No screening test in DM, risk is only 0.6%
• In pts with fish allergy skin testing is predictive,give 1mg prota diluted in
50ml over 10min & if no adverse response give full dose
• In pts with prior reaction to prota skin testing, RAST, ELISA appropriate,
test dose as before, use prota alternatives
Adverse Reactions
TREATMENT
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Slow adm limits Type III since large complexes do not form
Stop prota infusion
Stop all cardiodepressant drugs
IV fluids, Calcium
Antihistaminics
Hydrocortisone/ Aminophylline
Adm of heparin bolus in an attempt to decrease hep-prota
complex size
• Ionodilators- Milrinone, Isoproterenol
• Avoid rechallenge with prota
• Reinstitute CPB
TERMINATION FROM BYPASS
• Ventilation has been re established.
• Venous return to pump decreased by
clamping the line.
• If cardiac performance non optimal then
additional blood from pump can be taken.
• When BP,CO,Preload optimal arterial pump
stopped,and venous canula removed.
• Aortic canula not to be removed until test
dose of protamine given.
OFF PUMP CORONARY ARTERY BYPASS
SURGERY
• OPCAB accounts fot 20-30% of all CAB surgeries.
• Performed through median sternotomy.
• Bypass grafts include right and left mammary
arteries,saphenous veins,and radial arteries.
• Special sternal retractors used.
• Fixation devices stabalise the area of heart.
• Verticlisation of apex done.
• Surgical visualisation with help of blower.
• Distal anastomoses then performed.
ANAESTHETIC CONSIDERATIONS
• Revolve around
haemodynamic
perturbations.
• Surface stabaliser and apical
displacement device
associated with dec. CO,Sv
and MAP.
• The above can also lead to
distortion of mitral valve
annulus.
• Rewarming not done.
MONITORING
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Standard ASA
Arterial Catheter
Central Venous A
Ischemia Monitoring
- EKG ST trend
- PA Catheter?
- TEE?
MONITORING DIFFICULTIES
• Haemodynamic changes treated with volume
expansion.
• Blood transfusion for high risk patients.
• Hypotension can be treated with
inotropes,volume expansion.
• NTG to be used cautiously.
• Worsening haemodynamic status or ecg
changes warrrant insertion of intracoronary
stents.
• Conversion of OPCAB to CABG with CPB an
option.
ADVANTAGES OF OPCAB
• There are several advantages to beating heart
surgery from the anesthesiologist's
perspective:
• The patient is extubated early, is not severely
anemic, is awake and breathing on his/her
own.
• There are no cannulation sites in large vessels
which can potentially bleed.
• Less hemodilution.
• Coagulopathies are uncommon.
OTHERS…
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Shorter postoperative hospital stays.
Shorter time with ventilatory support.
Less blood loss and need for transfusions.
Less likelihood of low output syndrome.
Reduced systemic inflammatory response.
Fewer arrhythmia and neurologic
postoperative complications.
• Potential cost savings.
THANX!!