Cardio Pulmonary Bypass

CARDIO PULMO NAR Y BYP AS S PRESENTOR : dr.rajesh MODERATOR : DR. VEENA

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DEFINITION HISTORICAL ASPECT GOALS OF CPB COMPONENTS OF CPB ASSEMBLY & CONDUCT OF CPB PATHOPHYSIOLOGY OF CPB EMERGENCE FROM CPB COMPLICATIONS OF CPB.

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”

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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 

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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

PUMPS 

ROLLER PUMP

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CENTRIFUGAL PUMP Used for  Forward flow  Cardioplegia delivery  Lv vent suction

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ROLLER PUMP 

Most commonly used.

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Uses Volume displacement to create forward blood flow. Non Pulsatile Blood Flow By compressing Plastic Tubing b/w Roller & Backing Plate

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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

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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)

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Flow Generator 

FLOW = RPM x BOOT CAPACITY [Lit.] x 2 RPM = Revolution of the pump head 2 = Two arms of the pump

DISADVANTAGE of PULSATILE FLOW

producing

Bubble Formation  Damage to Blood Components. 

ADVANTAGE : ω ω

Improved Tissue Perfusion Better Preservation of Organ Function (Brain , Kidney)

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Roller Pumps are Electrically driven ; maintaining constant speed. Electric Failure → Hand driven.

CENTRIFUGAL PUMP Series of CONES that spin & propel blood forward by Centrifugal Force.  Safe  Reliable  Disposable  Simple to operate. 

CENTRIFUGAL PUMP 

ADVANTAGE

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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

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DISADVANTAGE

Inability to generate pulsatile flow  Potential discrepancy b/w pump speed & actual flow generated. 

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Preferred over roller pumps in Long-term CPB In high-risk angioplasty patients Ventricular assistance Neonatal ECMO

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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.

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Two Types :

 BUBBLE

OXYGENATOR  MEMBRANOUS OXYGENATOR

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BUBBLE OXYGENATOR     

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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  

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ADVANTAGE Easy to assemble Relatively small priming Volumes Adequate oxygenating capacity Lower cost.

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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.

 Bubble

oxygenators are not used for extended CPB times

MEMBRANOUS OXYGENATOR  

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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 DISADVANTAGE

ADVANTAGE

Can deliver AirO2 mixtures.  ↓Hemolysis  ↓ Protein desaturation  ↓ Post-op bleeding  Better platelet preservation. 

Expensive  Large priming volume  Prolonged use → pores may get blocked. 

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Factors affecting blood trauma in oxygenators are shear and stasis

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To optimise flow patterns COMPUTATIONAL FLUID DYNAMICS is used to design oxygenators

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. 

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

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MECHANICAL SUCTION Not desirable o Entrain Air o Suck the walls of the cavae against the orifices of the cannulae.

Size of cannula Adults

Children

SVC

28G

24G

IVC

36G

28G

TUBINGS IN THE CIRCUIT 

Non thrombogenic , Chemically Inert to prevent ω clotting ω Trauma to blood elements ω Protein Denaturation

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Smooth Internal Finish Non Reactable Internal Surface Durable to withstand high pressure & use of Roller pump

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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 

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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 œ Maintain Low LA & Pul.Venous Pressure œ Remove air from Cardiac Chamber. œ

•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. 

TWO TYPES 

Hard shell-open to atmosphere-superior in handling air from cardiotomy/vent returns

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Soft-shell-closes upon itself on emptying

CARDIOTOMY RESERVOIR 

For draining blood from LV/pul.artery/aortic root/surgical site via suction lines

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Blood is returned to venous reservoir

HEAT EXCHANGER 

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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  

Ascending Aorta just proximal to Innominate Artery. Femoral Artery in

Dissecting Aortic Aneurysm  For Reoperation  Emergency 

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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.

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MICROPORE FILTERS: Remove Particulate Matter (Bone , Tissue , Fat , Blood Clots etc.) Pore Size : 30 – 40 µ 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.

ADVANTAGE OF HEMODILUTION 

Lowers Blood Viscosity ⇒↓ in

Hematocrit.  Improves Microcirculation.  Counteracts the ↑ Viscosity by Hypothermia.

RISKS OF HEMODILUTION  

↓Viscosity - ↓ SVR - ↓ BP Low Colloid Oncotic Pressure - ↑ed Fluid

Requirement & Tissue Edema. 

O2 carrying Capacity ↓

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↓ Blood O2 content ⇒ Ischaemia of Critical

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Organs. Mixed Venous PO2 is ↓

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Dilution of Coagulation Factors.

COMPOSITION OF PRIME : Balanced salt soln. RL  Osmotically active agent

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(Mannitol, Dextran 40 , Hexastarch)  NaHCO3  KCl  Heparin

1250 ml 100 ml 50ml 10ml 1ml

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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 THREE MAJOR PHYSIOLOGICAL ABERRTIONS ARE: 1.LOSS OF PULSATILE FLOW 2.EXPOSURE OF BLOOD TO NONPHYSIOLOGIC SURFACES & SHEAR STRESSES. 3.EXAGGERATED STRESS RESPONSE. 

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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  ιι.

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 ιιι.

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portions of microvasculature. ↑ Catecholamines VC d/t hypothermia.

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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 

(A-a)O2 ↑ after CPB

 Max

after 18-48 hrs.  D/t : V-P imbalance  ↑in Pul. Interstitial fluid .

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

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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.

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 ↑

PREPARATION FOR CPB  

ANTICOAGULATION : M C used : Heparin  Rapid onset of action  Easy reversibility  Moderate therapeutic window  Few side effects.

 ABSOLUTE

C/I : HEPARIN INDUCED THROMBOCYTOPENIA.

HEPARIN     

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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

Heparin acts thru ANTITHROMBIN III (Naturally occurring anticoagulant)  Dose : loading dose 3mg/Kg 

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Causes of HEPARIN RESISTANCE Ongoing active coagulation AT III Deficiency. Prior heparin treatment Drug interaction (OCP) Advanced Age IV Nitroglycerine.

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

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ACTs

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<180 s - life threatening

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180-300 s -highly questionable

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>600 s –risky and unwise

PREBYPASS PREPARATION 

PERFUSIONIST

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ANAESTHESIOLOGIST

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SURGEON

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ARTERIAL CANNULATION is done Istleast hemodynamic changes. Anesthetic agent is given to overcome the dilutional effect of CPB

INITIATING CPB 

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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.

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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

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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

PERFUSIONIST  

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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 

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

 CVP 

& PCWP :

Should be near ZERO

 ↑SVC Pressure ⇒compromised cerebral 

circulan ↑PCWP / LA pressure ⇒LV Distension & possible myocardial damage.

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RECTAL & NASOPHARYNGEAL TEMPERATURE ECG :  To detect Residual Electrical Activity  Need for additional increments for cold cardioplegic solun U.O. : Maintained at 1ml/kg/hr ABG ESTIMATION HEMATOCRIT : 20-30 MONITOR & MAINTAIN THE ANTICOAGULATION.

CHECKLIST BEFORE SEPARATION FROM CPB 

Cardiac  Surgical  Bleeding  Valve function(TEE)  Intracardiac Air (TEE)  Aorta (TEE,confirm no Dissection )

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Rate , rhythm (ECG ) Ischaemia (ECG) Myocardial Function (Visual , TEE , C.O.) Temperature Hematocrit Electrolyte , acid – base status Ventilation , oxygenation

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

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Mech.Ventillation restored with 100% O2

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Venous drainage lines are gradually occluded,allowing arterial return to raise the circulatory volume.

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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  

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.

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SIS :BP is zero /low or increased line pressure is seen by perfusionist. TEE also useful. Prevention:BP should be lowered during Cannulation & Decannulation

 Treatment   

Stop the pump. Repositioning of aortic cannulae Repair of Dissection.

Arterial Cannulae Malposition 

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Results in Carotid /Innominate artery Hyperperfusion Detected by low left radial /femoral artery pressures Ipsilateral blanching of the face Ipsilateral Pupil Dilatation.

CANNULA REVERSAL 

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If the venous drainage is connected to arterial cannula & the arterial inflow to the venous drainage , the result would be catastrophic. Diagnosis :   

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Arterial Hypotension Facial edema Severe venous congestion

Reversed by terminating CPB Deep Trendlenburg Position Cannula & tubings properly connected.

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     

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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.

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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. Steroids administered Patient is weaned from CPB & ventilated with 100% O2 for atleast 6 Hrs.

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