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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 Ventillation Oxygenation CIRCULATION 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 OXYGENATOR Heat exchanger Arterial filter Cardioplegia delivery system Aortic/atrial/vena caval cannulae Suction/vent Slide 9: RESERVOIR PATIENT ARTERIAL LINE FILTER ROLLER PUMP OXYGENATOR HEAT EXCHANGER PUMPS : PUMPS ROLLER PUMP CENTRIFUGAL PUMP Used for Forward flow Cardioplegia delivery 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. ADVANTAGE : 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. Safe Reliable Disposable 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 Long-term CPB In high-risk angioplasty patients Ventricular assistance Neonatal ECMO Slide 25: Pressure-regulated pump Operates under passive filling After&pre-load sensitive Pump-chamberof polyurethane+peristaltic pump Not yet fully evaluated OXYGENATOR : OXYGENATOR Where O2 & CO2 Exchange takes place. Two Types : BUBBLE OXYGENATOR 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 Micro emboli 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: SOLID: Silicone MICROPOROUS: polypropylene,Teflon &polyacrylamide MEMBRANOUS OXYGENATOR : 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. 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 Entrain Air 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 clotting Trauma to blood elements Protein Denaturation Smooth Internal Finish Non Reactable Internal Surface Durable to withstand high pressure & use of Roller pump Slide 49: Made of PVC Polyurethane Silicone 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 More spallation 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 For Reoperation Emergency Problems of Femoral Cannulation : Sepsis 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 ULTRAFILTRATION : 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 Incompatibility Reactions. Demand on Blood Banks. Addition of Priming Fluid HEMODILUTION. ADVANTAGE OF HEMODILUTION : ADVANTAGE OF HEMODILUTION Lowers Blood Viscosity in Hematocrit. Improves Microcirculation. 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) NaHCO3 50ml KCl 10ml 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. Catecholamines 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 : Air Preexisting thrombi Platelet & leucocyte aggregate Fat globules Hemodilution –> mild cerebral edema CBF when MAP es <40mmHg during CPB RENAL EFFECT : RENAL EFFECT MICRO EMBOLI Vasoconstrictors 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 Easy reversibility 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) Advanced Age 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 ANAESTHESIOLOGIST 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 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 : CHECKLIST BEFORE SEPARATION FROM CPB Cardiac Surgical Bleeding Valve function(TEE) Intracardiac Air (TEE) Aorta (TEE,confirm no Dissection ) Rate , rhythm (ECG ) Ischaemia (ECG) Myocardial Function (Visual , TEE , C.O.) Temperature Hematocrit 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 Treatment 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. Diagnosis : Arterial Hypotension Facial edema 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. Steroids administered Patient is weaned from CPB & ventilated with 100% O2 for atleast 6 Hrs. THANK YOU : THANK YOU You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.