CARDIO

PULMO NAR Y
BYP AS S

PRESENTOR : dr.rajesh
MODERATOR : DR. VEENA
 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”
 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
 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

 CENTRIFUGAL PUMP
 Used for
 Forward flow
 Cardioplegia delivery
 Lv vent suction
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)
555
 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
 Bubble Formation
 Damage to Blood Components.

ADVANTAGE :
ω Improved Tissue Perfusion
ω Better Preservation of Organ Function (Brain ,
Kidney)
 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  DISADVANTAGE
ℵ No back pressure when
tubing is temporarily
 Inability to generate
obstructed / kinked pulsatile flow
ℵ Doesn’t produce spatulated
emboli from compression of  Potential discrepancy
the tubing b/w pump speed &
ℵ Cannot pump large amt.of
gas / gas emboli. actual flow generated.
ℵ Less blood trauma
ℵ High vol. output with
moderate pressures
 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 :

 BUBBLEOXYGENATOR
 MEMBRANOUS OXYGENATOR
555
5
 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 DISADVANTAGE
 Easy to assemble  Micro emboli
 Relatively small  Blood cell trauma
priming Volumes  Destruction of
 Adequate plasma protein due
oxygenating capacity to gas interface.
 Lower cost.  Excessive removal of
CO2
 Defoaming capacity
may get exhausted
with time.
 Bubbleoxygenators are not
used for extended CPB times
 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 DISADVANTAGE
 Can deliver Air-  Expensive
O2 mixtures.  Large priming
 ↓Hemolysis
volume
 ↓ Protein
 Prolonged use →
desaturation
pores may get
 ↓ Post-op
blocked.
bleeding
 Better platelet
preservation.
 Factors affecting blood trauma in
oxygenators are shear and stasis

 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.
 Blood flow ⇒Oxygenator (↓Gravity)
 Height Difference B/w Venacavae &
Oxygenator > 20-30 cm.
 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
 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
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
œ Keep the operative field clear
œ Maintain Low LA & Pul.Venous Pressure

œ 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.
TWO TYPES

 Hard shell-open to atmosphere-superior in

handling air from cardiotomy/vent returns

 Soft-shell-closes upon itself on emptying

CARDIOTOMY RESERVOIR

 For draining blood from LV/pul.artery/aortic

root/surgical site via suction lines

 Blood is returned to venous reservoir

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
 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
 Is the Narrowest part of the circuit.
 Should be as Short as possible.
 As Large as the diameter of vessel permits.
555
 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 ↓
 ↓ Blood O2 content ⇒ Ischaemia of Critical
Organs.
 Mixed Venous PO2 is ↓
 Dilution of Coagulation Factors.
COMPOSITION OF PRIME :

 Balanced salt soln. RL 1250 ml

 Osmotically active agent 100 ml
(Mannitol, Dextran 40 , Hexastarch)
 NaHCO3 50ml
 KCl 10ml
 Heparin 1ml
 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 NON-
PHYSIOLOGIC SURFACES & SHEAR
STRESSES.
3.EXAGGERATED STRESS RESPONSE.
 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
 SVR : Initial Phase SVR ↓
ιι. ↓ Blood Viscosity 20 to Hemodilution.
↑Vascular Tone d/t dilution of
ιιι.
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.
 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
 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
 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

 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
 ACTs

 <180 s - life threatening

 180-300 s -highly questionable

 >600 s –risky and unwise

PREBYPASS PREPARATION
 PERFUSIONIST

 ANAESTHESIOLOGIST

 SURGEON
 ARTERIAL CANNULATION is done Ist-
least hemodynamic changes.
 Anesthetic agent is given to overcome the
dilutional effect of 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.
 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
 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
 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.
 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 )
 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
 Mech.Ventillation restored with 100% O2
 Venous drainage lines are gradually
occluded,allowing arterial return to raise the
circulatory volume.
 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.
 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

 Results in Carotid /Innominate artery

Hyperperfusion
 Detected by low left radial /femoral artery
pressures
 Ipsilateral blanching of the face
 Ipsilateral Pupil Dilatation.
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
 CAUSES :
 Pumping Air thru an empty Reservoir ,
 Low reservoir level
 Disconnection with in the CPB
 Reversal of Pump head tubing
 Clotted Oxygenator.
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.
 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