CARDIO PULMONARY BYPASS : CARDIO PULMONARY BYPASS PRESENTOR : dr.rajesh
MODERATOR : DR. VEENA Slide 2: DEFINITION
GOALS OF CPB
COMPONENTS OF CPB
ASSEMBLY & CONDUCT OF CPB
PATHOPHYSIOLOGY OF CPB
EMERGENCE FROM CPB
COMPLICATIONS OF CPB. DEFINITION : 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 : 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 : 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 : GOALS OF CPB RESPIRATION
TEMP. REGULATION (Hypothermia)
Low blood flowso ed blood trauma
ses Body Metabolism. COMPONENTS OF CPB : 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 : INTEGRAL COMPONENTS OF extracorporeal circuit PUMPS
Cardioplegia delivery system
Aortic/atrial/vena caval cannulae
Suction/vent Slide 9: RESERVOIR PATIENT ARTERIAL
EXCHANGER PUMPS : PUMPS ROLLER PUMP
Lv vent suction ROLLER PUMP : 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 Slide 16: 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 Slide 17: 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) 555 : 555 Flow Generator : Flow Generator FLOW = RPM x BOOT CAPACITY [Lit.] x 2
RPM = Revolution of the pump head
2 = Two arms of the pump DISADVANTAGE of producing PULSATILE FLOW : DISADVANTAGE of producing PULSATILE FLOW Bubble Formation
Damage to Blood Components.
Improved Tissue Perfusion
Better Preservation of Organ Function (Brain , Kidney) Slide 21: Roller Pumps are Electrically driven ; maintaining constant speed.
Electric Failure Hand driven. CENTRIFUGAL PUMP : CENTRIFUGAL PUMP Series of CONES that spin & propel blood forward by Centrifugal Force.
Simple to operate. CENTRIFUGAL PUMP : 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. Slide 24: Preferred over roller pumps in
In high-risk angioplasty patients
Neonatal ECMO Slide 25: Pressure-regulated pump
Operates under passive filling
Pump-chamberof polyurethane+peristaltic pump
Not yet fully evaluated OXYGENATOR : OXYGENATOR Where O2 & CO2 Exchange takes place.
Two Types :
MEMBRANOUS OXYGENATOR 555 : 555 5 : 5 BUBBLE 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 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 : BUBBLE OXYGENATOR ADVANTAGE
Easy to assemble
Relatively small priming Volumes
Adequate oxygenating capacity
Lower cost. DISADVANTAGE
Blood cell trauma
Destruction of plasma protein due to gas interface.
Excessive removal of CO2
Defoaming capacity may get exhausted with time. Slide 35: Bubble oxygenators are not used for extended CPB times MEMBRANOUS OXYGENATOR : 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:
MICROPOROUS: polypropylene,Teflon &polyacrylamide MEMBRANOUS OXYGENATOR : MEMBRANOUS OXYGENATOR ADVANTAGE
Can deliver Air-O2 mixtures.
Better platelet preservation. DISADVANTAGE
Large priming volume
Prolonged use pores may get blocked. Slide 41: Factors affecting blood trauma in oxygenators are shear and stasis
To optimise flow patterns COMPUTATIONAL FLUID DYNAMICS is used to design oxygenators CIRCUITS : CIRCUITS Drains Venous Blood by gravity into oxygenator & returns the oxygenated blood under pressure to the systemic circulation. VENOUS DRAINAGE : 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. Slide 45: MECHANICAL SUCTION Not desirable
Suck the walls of the cavae against the orifices of the cannulae. Size of cannula : Size of cannula TUBINGS IN THE CIRCUIT : TUBINGS IN THE CIRCUIT Non thrombogenic , Chemically Inert to prevent
Trauma to blood elements
Smooth Internal Finish
Non Reactable Internal Surface
Durable to withstand high pressure & use of Roller pump Slide 49: Made of
I.D . Ranges from 3/16- 5/8 inches
HEPARIN BONDED CIRCUITS ARE AVAILABLE Slide 50: Disadvantages of plain circuits
Activation of platelets/coagulation factors
Post-op consumptive coagulopathyimmune reactions
Heparin coated circuits are
More hemo compatible
Cause less activation of platelets/white cells
Reduce heparin demand INTRACARDIAC SUCTION : INTRACARDIAC SUCTION Blood will enter the heart
Coronary venous Return
Retrograde flow in AR.
Bronchial Arteries CARDIOTOMY SUCTION : CARDIOTOMY SUCTION Spilled Heparinised Blood is Scavenged & returned back to patient.
Handheld Suckers are used to return this blood. VENTRICULAR VENTING : 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 : 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. Slide 55: TWO TYPES
Hard shell-open to atmosphere-superior in handling air from cardiotomy/vent returns
Soft-shell-closes upon itself on emptying Slide 56: CARDIOTOMY RESERVOIR
For draining blood from LV/pul.artery/aortic root/surgical site via suction lines
Blood is returned to venous reservoir HEAT EXCHANGER : HEAT EXCHANGER Water at a predetermined Temp. spiral coils & Patients Blood in the opposite directn using Counter – Current Mechanism.
Often an integral part of the oxygenator
Usual range is 4 - 42 deg.celsiusheat transfer by conduction
Risk of aluminium leaching into blood ARTERIAL RETURN : ARTERIAL RETURN Ascending Aorta just proximal to Innominate Artery.
Femoral Artery in
Dissecting Aortic Aneurysm
Problems of Femoral Cannulation :
Formation of False Aneurysm
Development of Lymphatic Fistula. ARTERIAL CANNULA : ARTERIAL CANNULA Is the Narrowest part of the circuit.
Should be as Short as possible.
As Large as the diameter of vessel permits. 555 : 555 Slide 61: MICROPORE FILTERS:
Remove Particulate Matter (Bone , Tissue , Fat , Blood Clots etc.)
Pore Size : 30 – 40
Remove the excess fluid from the CPB. PRIME FLUID : PRIME FLUID Ideally close to ECF.
Whole Blood NOT used :
Homologous Blood Syndrome.
Post Perfusion Bleeding Diathesis
Demand on Blood Banks.
Addition of Priming Fluid HEMODILUTION. ADVANTAGE OF HEMODILUTION : ADVANTAGE OF HEMODILUTION Lowers Blood Viscosity in Hematocrit.
Counteracts the Viscosity by Hypothermia. RISKS OF HEMODILUTION : RISKS OF HEMODILUTION Viscosity - SVR - BP
Low Colloid Oncotic Pressure - ed Fluid Requirement & Tissue Edema.
O2 carrying Capacity
Blood O2 content Ischaemia of Critical Organs.
Mixed Venous PO2 is
Dilution of Coagulation Factors. COMPOSITION OF PRIME : : COMPOSITION OF PRIME : Balanced salt soln. RL 1250 ml
Osmotically active agent 100 ml
(Mannitol, Dextran 40 , Hexastarch)
Heparin 1ml Slide 66: Blood is added if calculated PCV after mixing with pt.’s blood is below 25%.
An avg. requirement of PRIME is 1500-2000ml. PATHOPHYSIOLOGY OF CPB : 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. Slide 68: 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.) CIRCULATORY SYSTEM : CIRCULATORY SYSTEM SVR : Initial Phase SVR
Blood Viscosity 20 to Hemodilution.
Vascular Tone d/t dilution of circulatory catecholamines
As CPB BP , d/t SVR
Actual in Vascular C/S area d/t closure of portions of microvasculature.
VC d/t hypothermia. Slide 70: 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 : PULMONARY EFFECT (A-a)O2 after CPB
Max after 18-48 hrs.
D/t : V-P imbalance
in Pul. Interstitial fluid
. PULMONARY EFFECT : 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 : CNS CHANGES Embolic phenomena :
Platelet & leucocyte aggregate
Hemodilution –> mild cerebral edema
CBF when MAP es <40mmHg during CPB RENAL EFFECT : RENAL EFFECT MICRO EMBOLI
Ppt. of Plasma Hb in Renal tubules U.O. HEMATOLOGIC EFFECT : 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 : 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: : 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 PREPARATION FOR CPB : PREPARATION FOR CPB ANTICOAGULATION :
M C used : Heparin
Rapid onset of action
Moderate therapeutic window
Few side effects.
ABSOLUTE C/I : HEPARIN INDUCED THROMBOCYTOPENIA. HEPARIN : HEPARIN Polyanionic mucopolysaccharides
Normal half time – 90-100 min
Highly protein bound
Metabolised by Hepatic Metabolism
Can also taken up by Endothelial cells ,where it is neither metabolised nor neutralised.
Dosage in CPB is determined empirically Slide 80: Heparin acts thru ANTITHROMBIN III (Naturally occurring anticoagulant)
Dose : loading dose 3mg/Kg
Causes of HEPARIN RESISTANCE
Ongoing active coagulation
AT III Deficiency.
Prior heparin treatment
Drug interaction (OCP)
IV Nitroglycerine. Slide 81: Protocol
Initial dose- 300u/kg
Arterial sample in 3-5 min
Give additional heparin as needed to maintain ACT >300 s in normothermic and >400 s in hypothermic CPB
Prime extracorporeal circuit with 3u/ml heparin
Monitor ACT every 30 min or more frequently if pt.is heparin resistant
If ACT goes <300 s give additional 50 u/kg heparin Slide 82: ACTs
<180 s - life threatening
180-300 s -highly questionable
>600 s –risky and unwise PREBYPASS PREPARATION : PREBYPASS PREPARATION PERFUSIONIST
SURGEON Slide 84: ARTERIAL CANNULATION is done Ist- least hemodynamic changes.
Anesthetic agent is given to overcome the dilutional effect of CPB INITIATING CPB : INITIATING CPB After making connections , CPB is commenced by removing the clampsin the venous line.
As the blood starts to fill up the reservoir of the oxygenator , th arterial pump is turned on & th flow gradually raised to the desired levels.
In AR patients Aortic Clamp is applied quickly to avoid overdistension of LV. Slide 86: Vent line is introduced thru LV Apex .
Until the encirciling tapes around SVC & IVC are tightened , a part of venous return will reach the heart chambers & pul. Cir.
This period is k/a PARTIAL BYPASS
Once the tapes are snared snugly over the venous cannulae TOTAL BYPASS begun.
Initial transient BP fall is seen Slide 87: VENTILLATION IS SUSPENDED WITH INITIATION OF TOTAL BYPASS .
Lungs may be kept inflated at 5-10cm of H2O/left open to the atmosphere.
Aorta is cross clamped & cardioplegic myocardial protection given before surgical correction is undertaken. MONITORING : MONITORING PERFUSIONIST : PERFUSIONIST VENOUS RETURN :
PUMP FLOW : maintained at 2.4L/min/m2
ARTERIAL LINE PRESSURE :
NEGATIVE SUCTION ON THE VENT & CARDIOTOMY SUCTION :
PERFUSATE TEMPERATURE :
ABG & ELECTROLYTE ESTIMATION : ANAESTHESIOLOGIST : ANAESTHESIOLOGIST SYSTEMIC BP : maintain at 70-80 mmHg
>100mmHg - es non coronary blood flow warming ischaemic myocardium , when Aorta is cross clamped /opened.
<50mmHg – higher incidence of neurological compln Slide 91: CVP & PCWP :
Should be near ZERO
SVC Pressure compromised cerebral circulan
PCWP / LA pressure LV Distension & possible myocardial damage. Slide 92: RECTAL & NASOPHARYNGEAL TEMPERATURE
To detect Residual Electrical Activity
Need for additional increments for cold cardioplegic solun
U.O. : Maintained at 1ml/kg/hr
HEMATOCRIT : 20-30
MONITOR & MAINTAIN THE ANTICOAGULATION. CHECKLIST BEFORE SEPARATION FROM CPB : CHECKLIST BEFORE SEPARATION FROM CPB Cardiac
Intracardiac Air (TEE)
Aorta (TEE,confirm no Dissection )
Rate , rhythm (ECG )
Myocardial Function (Visual , TEE , C.O.)
Electrolyte , acid – base status
Ventilation , oxygenation WEANING FROM CPB : WEANING FROM CPB Adequately REWARMED.
Myocardial contractility & Rhythm monitored .
Restore the lung ventillation initially by Positive Pressure Ventillation.(20-40 cm of H2O) to reinflate area of Atelectasis
Mech.Ventillation restored with 100% O2
Venous drainage lines are gradually occluded,allowing arterial return to raise the circulatory volume. Slide 95: When sufficient volume has been transferred to optimise preload , BP & CO ,arterial pump is stopped.
Venous cannulae are removed
Protamine administered to Neutralise Heparin (6mg/Kg)
Aortic Cannula is left insitu for rapid transfusion , until the anticoagulation is reversed .
Removal of Aortic Cannula is the final step in the termination of CPB. COMPLICATIONS OF CPB : COMPLICATIONS OF CPB AORTIC DISSECTION :
OCCURS DURING CANNULATION PROCESS,WHEN THE CANNULA CAUSES A SEPARATION OF THE INTIMAL WALL FROM THE MEDIA & ADVENTIA,THEREBY CREATING A FALSE LUMEN. Slide 97: SIS :BP is zero /low or increased line pressure is seen by perfusionist.
TEE also useful.
Prevention:BP should be lowered during Cannulation & Decannulation
Stop the pump.
Repositioning of aortic cannulae
Repair of Dissection. Arterial Cannulae Malposition : Arterial Cannulae Malposition Results in Carotid /Innominate artery Hyperperfusion
Detected by low left radial /femoral artery pressures
Ipsilateral blanching of the face
Ipsilateral Pupil Dilatation. CANNULA REVERSAL : CANNULA REVERSAL If the venous drainage is connected to arterial cannula & the arterial inflow to the venous drainage , the result would be catastrophic.
Severe venous congestion
Reversed by terminating CPB
Deep Trendlenburg Position
Cannula & tubings properly connected. MASSIVE GAS EMBOLISM : MASSIVE GAS EMBOLISM CAUSES :
Pumping Air thru an empty Reservoir ,
Low reservoir level
Disconnection with in the CPB
Reversal of Pump head tubing
Clotted Oxygenator. Treatment Protocol : Treatment Protocol Stop CPB
Place the patient in steep Trendlenburg position
Remove aortic cannula,vent the air from aortic cannula site
De-air arterial line & pump line
Institute the hypothermic retrograde SVC perfusion by connecting arterial pump line to svc cannula & the air + blood is drained from the Aortic Root.
Carotid compression intermittently to allow retrograde purging of air from the vertebral arteries. Slide 102: Retrograde IVC perfusion done in extensive systemic air injection.
Ante grade CPB should be resumed & Hypothermia should be maintained for forty five min.
Induce Hypertension with Vasoactive drugs
Express the coronary air by massaging & needle venting.
Patient is weaned from CPB & ventilated with 100% O2 for atleast 6 Hrs. THANK YOU : THANK YOU