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 VentillationOxygenationCIRCULATIONTEMP. REGULATION (Hypothermia)Low blood flowso ed blood trauma ses Body Metabolism.

COMPONENTS OF CPB

• TOTAL CPB : Systemic venous drainage CPB Circuit External oxygenator heat exchanger External pump arterial filterSystemic 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 exchangerArterial filterCardioplegia delivery systemAortic/atrial/vena caval cannulaeSuction/vent

RESERVOIR

PATIENTARTERIAL

LINEFILTER

ROLLERPUMP

OXYGENATORHEAT

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 :w Improved Tissue Perfusionw 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• ADVANTAGEÀ No back pressure when tubing

is temporarily obstructed / kinked

À Doesn’t produce spatulated emboli from compression of the tubing

À Cannot pump large amt.of gas / gas emboli.

À Less blood traumaÀ 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 byDirect 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 wclottingwTrauma to blood elementswProtein 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

x 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 AneurysmFor 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 1250 ml

• Osmotically active agent 100 ml (Mannitol, Dextran 40 , Hexastarch)

• NaHCO3 50ml

• KCl 10ml• Heparin 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 = Pt. RBC volume before CPB

/ Pt. EBV + CPB prime volume

– EBV • Infants 80-85 ml/kg• Children 75ml/kg• Adult (male) 70ml/kg• Adult (female) 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 catecholaminesAs CPB BP , d/t SVRa) Actual in Vascular C/S area d/t closure of portions of

microvasculature.b) Catecholaminesc) 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 status1. High dose opioid anesthesia2. Total intravenous anesthesia3. Mixed iv/inhalational agent anesthesia

• High dose opioid• Fentanyl -50-100mic/kg,sufentanil 15-25mic/kgADV-Faster extubationDisadvantage-1. Prolonged respiratory depression2. Chest wall ridgidity3. Patient awareness4. Inability to control hypertensive response

Total iv anaesthesia• Propofol 1-2 mg/kg with infusion of 50-

100mic/kg/min• Remifentanil 0-1mic/kg bolus followed by .25-

1mic/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-CPBTwo 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, LIMA

dissection, CPB venous cannulation. • Decrease HR, BP, ischemia, dysrhythmias

• 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% N-

acetylation.

• 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

• Previous heparin therapy

• OCP/ Pregnancy

• Thrombocytosis

• Congenital AT-III deficiency• Hemodilution

• IABP• Shock• STK• Infective endocarditis• Ventricular aneurysm with

thrombus• Consumptive coagulopathy

• 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 an unrecognized endothelial heparin

antagonist– more rapid clearance of protamine to heparin.

• Incidence-50%• Can occur as soon as 1 hr after prota adm

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 –350CModerate - 26-310CDeep 18-260CProfound - <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, freeradicals,metalloproteinases

• Systemic inflammatory response to bypass

MONITORING

PATIENT• ECG

• Arterial/ Perfusion pr

• Coagulation-ACT,TEG

• SpO2 ,EtCO2

• ABG

• BSL

• EEG, BIS

• CVP/ PAC • Temperature• Urine output• Se electrolytes• Hb, Hct• TEE• SjvO2

•

PUMP

Inline blood gas monitoring

Venous oximetry

Line pressure

Temperature monitoring

Flow

Reservoir volume

Bubbles

CARDIOPLEGIARoute• 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 • intermittent

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 CPBC 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

• 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

• 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…

• 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!!