ANAESTHETIC CONSIDERATIONS IN CPB

Moderator-Dr.Surinder Singh

By-Dr Suchit KhandujaJR ANAESTHESIA

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.

DEFINITION

Legllois (1812) : “circulation might be taken over for short periods”

The first heart-lung machine was built by physician, John Heysham Gibbon in 1937

Dr. Clarence Dennis led the team that conducted the first known operation involving open cardiotomy with temporary mechanical takeover of both heart and lung functions on April 5, 1951 at the University of Minnesota Hospital.

Dr.John Gibbon(Philadelphia) 1953 :

“performed ASD repair with the aid of CPB for the 1st time with the survival of patient.”

HISTORICAL ASPECTS

GOALS OF CPBTo provide a still &

Bloodless Heart with blood flow temporarily diverted to an Extracorporeal Circuit that functionally replaces the Heart & the Lung

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.

COMPONENTS OF CPB

PUMPS OXYGENATOR Heat exchangerArterial filterCardioplegia delivery systemAortic/atrial/vena caval cannulaeSuction/vent

INTEGRAL COMPONENTS OF extracorporeal circuit

RESERVOIR

PATIENT

ARTERIAL LINE

FILTER

ROLLERPUMP

OXYGENATORHEAT

EXCHANGER

Most commonly used.Uses Volume displacement to create forward blood flow.Non Pulsatile Blood FlowBy compressing Plastic Tubing b/w Roller & Backing Plate

ROLLER PUMP

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

Bubble Formation Damage to Blood Components.

ADVANTAGE :wImproved Tissue PerfusionwBetter Preservation of Organ Function (Brain , Kidney)

DISADVANTAGE of producing PULSATILE FLOW

Series of cones that spin & propel blood forward by Centrifugal Force.

Safe ReliableDisposableSimple 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.

CENTRIFUGAL PUMP

Preferred over roller pumps inLong-term CPB

In high-risk angioplasty patients

Ventricular assistance

Neonatal ECMO

Pressure-regulated pumpOperates under passive filling

After&pre-load sensitive

Pump-chamberof polyurethane+peristaltic pump

Not yet fully evaluated

OXYGENATORWhere O2 & CO2 Exchange takes place.Two Types :

BUBBLE OXYGENATOR

MEMBRANOUS OXYGENATOR

BUBBLE OXYGENATORGas 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 columnLarger 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

BUBBLE OXYGENATOR ADVANTAGEEasy to assembleRelatively small

priming VolumesAdequate

oxygenating capacity

Lower cost.

DISADVANTAGEMicro emboliBlood cell traumaDestruction 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 membraneEliminates the need for a bubble-blood contact & need for a

defoamer; so more physiological.Blood damage is minimumIdeal for perfusions lasting for >2-3 hours.2 types of membrane:SOLID: Silicone MICROPOROUS: polypropylene,Teflon &polyacrylamide

MEMBRANOUS OXYGENATOR ADVANTAGECan deliver Air-O2

mixtures.Hemolysis Protein desaturation Post-op bleedingBetter platelet

preservation.

DISADVANTAGEExpensiveLarge priming volumeProlonged use pores

may get blocked.

CIRCUITS†Drains Venous Blood by gravity into

oxygenator & returns the oxygenated blood under pressure to the systemic circulation.

VENOUS DRAINAGESystemic venous blood (Rt.Heart)to Oxygenator by

Direct Cannulation of SVC & IVC (Bicaval Cannulation) thru RA & joined to create a single drainage channel.

Single cannula into RA thru RA appendageMostly RA cannulation doneBicaval cannulation done is procedure such as

MVR.

Blood flow to Oxygenator (Gravity)Height Difference B/w Venacavae & Oxygenator > 20-30 cm.

arrhythmia

bleeding

ivc/svc tear

cannula malposition

low return

inadequate height

malposition

kink,clamp,air lock

Complications

Size of cannula

Adults Children

SVC 28FG 24FG

IVC 36FG 28FG

TUBINGS IN THE CIRCUITMade of PVC,Polyurethane,SiliconeI.D . Ranges from 3/16- 5/8 inches

Non thrombogenic , Chemically Inert to prevent clottingTrauma to blood elementsProtein Denaturation

Smooth Internal FinishNon Reactable Internal SurfaceDurable to withstand high pressure & use of Roller pump

Disadvantages of plain circuitsActivation of platelets/coagulation factorsPost-op consumptive coagulopathyimmune reactionsMore spallation

Heparin coated circuits areMore hemo compatibleCause less activation of platelets/white cellsReduce heparin demand

INTRACARDIAC SUCTIONBlood will enter the heart

Coronary venous ReturnRetrograde flow in AR.Bronchial Arteries

CARDIOTOMY SUCTIONSpilled Heparinised Blood is Scavenged & returned back to

patient.Handheld Suckers are used to return this blood.

VENTRICULAR VENTING Done by passing the vent from superior pulmonary vein to LA to

left ventricleCan also be done through Aortic rootBlood from LV flows to Reservoir Bag LV Venting done to

Keep the operative field clearMaintain Low LA & Pul.Venous PressureRemove air from Cardiac Chamber.

Blood from LV Reservoir Bag

RESERVOIR BAGCollects the blood from venous drainage and cardiotomy suction

passively

Blood reservoirs may be collapsible plastic bags or clear plastic hard-shelled containers.

Hard-shelled reservoirs include an integral filtration mechanism with a screen and depth filters through which blood must pass before leaving the outlet of the vessel.

Volume in the bag should not be allowed to empty to prevent massive emboli.

ARTERIAL RETURNAscending 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.Axillary artery cannualtion done in surgeries involving aortic

arch

ARTERIAL CANNULA Is the Narrowest part of the circuit.

Should be as Short as possible.

As Large as the diameter of vessel permits.

ComplicationsDifficult 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 DiathesisIncompatibility 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

PRIMINGHeme, 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.)

THREE MAJOR PHYSIOLOGICAL ABERRTIONS ARE:1.LOSS OF PULSATILE FLOW

2.EXPOSURE OF BLOOD TO NON-PHYSIOLOGIC SURFACES & SHEAR STRESSES.

3.EXAGGERATED STRESS RESPONSE.

PATHOPHYSIOLOGY OF CPB

SVR : Initial Phase SVR .i Blood Viscosity 20 to Hemodilution.

ii. Dec 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 Catecholamines

c) VC d/t hypothermia.

Cardiac output : flow rate at 2.2-2.4 l/m2/min at 370c.BP : 50- 80mm hgVenous tone : Close to zero

CIRCULATORY SYSTEM

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 CHANGESEmbolic phenomena :

AirPreexisting thrombiPlatelet & leucocyte aggregateFat globules

Hemodilution –> mild cerebral edemaCBF when MAP es <40mmHg during CPB

RENAL EFFECTMICRO 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 Inc Hemolysis d/t high flow rates

WBC : Marked DEC in PMN

PLATELETS : aggregation & dysfunction, can also lead to thrombocytopenia.

HEMATOLOGIC EFFECT

PLASMA PROTEIN :DenaturationAltered enzymatic functionAggregation of plateletsAltered solubility characteristicsRelease of lipidsAbsorption 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 ANAESTHESIAChoice depends on haemodynamic status1. High dose opioid anesthesia2. Total intravenous anesthesia3. Mixed iv/inhalational agent anesthesia

High dose opioidFentanyl -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 anaesthesiaPropofol 1-2 mg/kg with infusion of 50-

100mic/kg/minRemifentanil 0-1mic/kg bolus followed by .25-

1mic/kg/minTCI may be used

Mixed IC/Inhalational anesthesiaInterest grew after studies on protective effect

of volatile agents on myocardiumPropofol,thiopentone,midazolam may all be

givenOpioid given in smaller dosages with

inhalational agent at .5-1.5 MACIsoflurane,sevoflurane and desflurane usedN2O 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 acidstrongest 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 ).

 

• 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.• 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 deficiencyHemodilution

• 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 tissuesdelayed return of heparin to circulation from extracellular space via

lymphaticsclearance of an unrecognized endothelial heparin antagonistmore 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.

.

HIT

Immune-mediated prothombotic disorder that occurs in patients exposed to heparin.

Antibodies form against the protein platelet factor 4 (PF4) when PF4 has formed a complex with heparin.

Presence of heparin increases plasma concentrations of PF4 15- to 30-fold by displacing bound PF4 on endothelial cell surfaces making it available to bind with heparin.

Binding of the resulting PF4-heparin complex to platelets leads to immunologically mediated platelet activation.

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.

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

Treatment

HEPARIN SUBSTITUTES

CANNULATION

Aortic cannula first Maintain SBP to 90-100MAP 60 –80Excessive 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

Complicationsarrhythmia

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) releaseDecreases 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 occurNodal, 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.

NORMOTHERMIC CPBWarm 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 32-340CTerminate CPB 34-350C

MEAN ARTERIAL PRESSUREmaintain 70-90 @ normothermia50-70 mm Hg 30-32°C30-40 mm Hg @ <30°C

Higher pressures- increased non coronary collateral flowMaintain adequate flowsSVR-

increased by phenylephrine, noradrdecreased by NTG, SNP, anaesthetics

CPB INFLAMMATORY RESPONSE

Blood contact with non endothelial surface

Complement system, monocyte- macrophage system, cytokines, endotoxins, freeradicals,metalloproteinases

Systemic inflammatory response to bypass

MONITORINGPATIENT

ECG

Arterial/ Perfusion pr

Coagulation-ACT,TEG

SpO2 ,EtCO2

ABG

BSL

EEG, BIS

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

• SvO2

•

PUMP

Inline blood gas monitoring

Venous oximetry

Line pressure

Temperature monitoring

Flow

Reservoir volume

Bubbles

CARDIOPLEGIARouteantegrade

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/ kgtarget myocardial temp. is 10-15ºC repeat every 20-30 mindose 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

WEANING FROM CPBC V P

Cold Ventilation Predictor

Conduction Visualisation Pressure

Cardiac output Vapourizer Pressors

Cells Volume expander Pacer

Calcium Potassium

Coagulation Protamine

PROTAMINEMeischer 1868, Hagedorn & colleagues 1936contains many positive charges, nearly 2/3rd arginineStable without refrigeration for several weeksAvailable 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 effectNeutralizes AT effect of heparin far better than anti Xa effect,

hence poor ability to neutralize LMWHs

Recommended doses to neutralize heparin vary widely

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

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

TREATMENT

Slow adm limits Type III since large complexes do not formStop prota infusionStop all cardiodepressant drugsIV fluids, CalciumAntihistaminicsHydrocortisone/ AminophyllineAdm of heparin bolus in an attempt to decrease hep-prota complex

sizeIonodilators- Milrinone, IsoproterenolAvoid rechallenge with protamineReinstitute CPB

Ventilation has been re established.Venous return to pump decreased by clamping the line.Ventricular distention should be avoided because it increases wall tension and

myocardial oxygen consumption.Pump flow into the aorta is lowered, in effect moving into a partial bypass phase If cardiac performance non optimal then additional blood from pump can be taken

with concomitant TEEWhen BP,CO,Preload optimal arterial pump stopped,and venous canula removed. Venous and Aortic canula not to be removed until test dose of protamine given.

TERMINATION FROM BYPASS

Awareness

Cardiovascular disturbance

Arrythmias

Pulmonary complications

Metabolic abnormalities

bleeding and coagulopathies

PROBLEMS AFTER CPB

Chest ClosureHemodynamic deterioration may occur

during chest closure TEE is often particularly useful in these

casesOccasionally sternum is not closed inOT Transport to ICUAnaesthesiologist must be actively involvedAll parametres should be continuously

monitored

THANX!!