CPB provides cardiopulmonary support during cardiac surgery by diverting blood flow away from the heart and through an external circuit that oxygenates the blood and returns it. John Gibbon performed the first successful open heart surgery using CPB in 1953. The key components of a CPB circuit include a venous reservoir, oxygenator, heat exchanger, pump, and arterial filter. Membranous oxygenators are now most commonly used due to reduced blood trauma compared to bubble oxygenators. Proper priming of the circuit is also important for safe initiation of CPB.

1. CPB- ANESTHESIA,
PHYSIOLOGICAL
EFFECTS, WEANING
MODERATOR – DR JAGDISH.A
SPEAKER- DR SINDHU PRIYA.M

3. INTRODUCTION
 CPB provides extracorporeal maintenance of
respiration & circulation at normothermic &
hypothermic temperatures. It diverts venous blood away
from the heart , adds oxygen , removes carbon dioxide ,
returns blood to a large artery[usually aorta]
 It stops nearly all blood flow in the heart, most blood
flow in the lungs

5. RESERVOIR
PATIENT
ARTERIAL
LINE
FILTER
ROLLER
PUMP
OXYGENATOR
HEAT
EXCHANGER

6. 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.”

7. Dr JOHN GIBBON Jr

8. • University of Minnesota was the place
where open heart surgery was developed
• Dr. John Lewis first closed ASD in a 5yr old
girl under direct vision using inflow stasis &
moderate hypothermia on Sep 2,1952.
• On may 6,1953 Dr. John Gibbon Jr first
used the pump oxygenator on a ASD pt
successfully.

9. FIRST ASD CLOSURE

10. 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

11.  FULL CPB—Venous blood is removed from the rt
heart &returned to the systemic circulation via the
aorta
 PARTIAL CPB—Used in thoracic aorta operations—
where only thoracic aorta is bypassed—oxygenated
blood is removed from the left side of the heart
&returned to the femoral artery.
 Here blood passes through the pulmonary
circulation , so oxygenator is not needed

12. COMPONENTS
• 1.Venous reservoir
• 2.Oxygenator
• 3.Heat exchanger
• 4.Main pump
• 5.Arterial filter
• -Modern machines have built in 1+2+3
• -The tubing is made of medical grade
PVC with a coating which alters bioactivity
of the surface

13.  Separate accessory devices —blood
salvage[ cardiotomy suction ],venting the
left ventricle , cardioplegia pump
 Filters, in line pressure gauges , oxygen
saturation monitors , temp monitors are
also used.

14. 1.RESERVOIR:
• Collapsible bags/hard shell containers with
filters& pressure relief valves
• High capacitance low pressure system
• Blood flows to reservoir due to gravity
• As venous pressure is low, the driving
pressure is directly proportional to the
difference in height between pt &
reservoir; inversely proportional to the
resistance of cannulas & tubing
• The fluid level in the reservoir is critical

17. OXYGENATOR
 Where O2 & CO2 Exchange takes place.
 Two Types :
 BUBBLE OXYGENATOR
 MEMBRANOUS OXYGENATOR

18. BUBBLE OXYGENATOR
 Gas exchange by directly infusing the gas into a column of
systemic venous blood.
 OXYGENATING CHAMBERS : Bubbles produced by
ventilating gas through diffusion plate into venous blood
column
 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

19.  Oxygen transfer is proportional to bubble
size and carbon dioxide exchange is
proportional to gas flow.
 Smaller bubbles are very efficient at
oxygenation but poor in Co2 removal

22. DEFOAMING CHAMBER
 Defoaming of frothy blood
 Large surface area coated with silicone
 This es the Surface Tension of the
bubbles causing them to burst.

23. 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.

24. MEMBRANOUS OXYGENATOR
 It has a membrane bt gas and blood phases
 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

25.  2 types of membrane:
SOLID: Silicone
MICROPOROUS: polypropylene , Teflon &
polyacrylamide

26.  It has a thin gas permeable membrane with micropores. It
is made of polypropylene—thin straws with outer
diameterof 200-400um,wall thickness of 20-50um,total
surface area-2-4m2 .[hollow fibre design,folded envelope
design]
 True membrane lungs are also used
 Control of PaO2 &PaCO2
 It can oxygenate 7L/min of venous blood
 Gas transfer depends on diffusion. Arterial oxygen tension
is inversely proportional to the thickness of the blood film
in contact with the membrane. Arterial CO2 tension is
directly proportional to total gas flow.
 As inspired O2 concentration can be varied, membrane
oxygenator allows independent

27.  Gas transfer is based on
Fick’s Law of Diffusion:
Volume of gas diffused=
Diffusion coefficient*Partialpressuredifference
----------------------------------------------------------
Distance of travel of gas
 Arterial oxygen tension is inversely proportional to the
thickness of the blood film in contact with the
membrane. Arterial CO2 tension is directly
proportional to total gas flow.
 As inspired O2 concentration can be varied, membrane
oxygenator allows independent control over pO2

30. 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.
 Single use

31. HEAT EXCHANGER
 Any time 20-35% of TBV is in CPB
 Blood from oxygenator enters heat exchanger where it
can be cooled or warmed depending on temperature of
water flowing through exchanger
 Heat transfer occurs by conduction
 At low temperatures the gas solubility increases
 So filters are built into unit to catch any bubbles
formed during rewarming.

33. Main pump
 Two types
• Roller pump
• Centrifugal pump

34. ROLLER PUMP
 Most commonly used.
 Uses Volume displacement to create forward blood
flow
 Pulsatile Blood Flow
 By compressing Plastic Tubing b/w Roller & Backing
Plate
 Independent of circuit resistance

36. 555

37. • Roller pump:
• Heads turn –compress large bore tubing in main
pumping chamber-producing flow. Subtotal occlusion of
tubing may produce RBC trauma.
• A constant speed of roller pumps produce a continuous
non pulsatile flow
• The flow is proportional to number of revolutions per
minute.
• They are placed after the oxygenator.
• In case of power failure all pumps have hand crank for
manual pumping, some pumps have emergency battery
back up
• Pulsatile flow is seen in roller pumps

38. CENTRIFUGAL PUMP:
 Has a series of cones in plastic housing. As cones spin –a
centrifugal force is created which propels blood from
centrally located inlet to periphery.
 Here flow is pressure sensitive
 If distal pressure is increased, then flow decreases so
pump speed must be increased.
 If pressure is increased excessively then back flow will
take place ,so unidirectional valves are placed
 These pumps are nonocclusive—so less RBC trauma
 Placed between reservoir &oxygenator

40. 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.

41. ARTERIAL FILTER
 A final inline arterial filter is placed in
the arterial cannula line . It is around 27-
40 um in size.
 It prevents entry of particulate matter
eg: thrombi,fat,calcium,tissue debris
 A filter always has a bypass limb which is
normally clamped. It is used if the filter
becomes clogged.
 It develops high resistance, if clogged.
Always measure arterial inflow pressure
before the filter

42. ACCESSORY DEVICES
• A] Cardiotomy suction:
• Aspirates blood from the operative field &returns to
the main pump reservoir
• A cell saver suction can also be used where blood is
returned to a separate reservoir—which at end of
procedure is centrifuged , washed,returned to the
patient—but if used in excess it depletes CPB circuit
volume
• If suction pressure is more—RBC trauma

43. CARDIOTOMY SUCTION

44. B] LV vent
 Even after total CPB is initiated—blood reaccumulates
in the LV [residual pulmonary flow from bronchial
artery, thebesian vessels, AR—structural & functional]
 LV distention myocardial stretching
increase in O2 demand dec subendocardial perfusion
 Venting can be achieved—catheter into LV via rt
superior pulmonary vein & LA ;via LV apex through
aortic valve
 Blood goes via vent pump—filters—returns to venous
reservoir

45. C] CARDIOPLEGIA PUMP
 By using a separate pump for cardioplegia, optimal
control over infusion pressure , rate, temperature is
achieved
 A separate heat exchanger is used to control temp of
cardioplegic solution or cold cardioplegic solution may
be given under pressure or by gravity

47. • D] ULTRAFILTER
• -It is used during CPB to increase pts hematocrit
without transfusion.
• Hydrostatic pressure drives the Ultrafiltration.
Effluents upto 40ml/min can be filtered.
• Heme ultrafilters made of hollow capillary fibres which
function as membranes
• They separate aqueous phase of blood from the
cellular & proteinaceous component
• Ultrafilters can receive blood from arterial /venous
side

49. CIRCUIT SELECTION &PRIMING
• The cardiopulmonary bypass (CPB) circuit must be
primed with a fluid solution, so that adequate flow
rates can be rapidly achieved on initiation of CPB
without risk of air embolism (de- air)
• Minimum safe priming volume - guided by the patient’s
weight or body surface area
• The minimum volume required is that which fills both
venous and arterial limbs of the circuit and maintains an
adequate reserve volume in the venous reservoir to
ensure that air is not entrained into the arterial side of
the circuit.

50.  In adults, priming volumes are 1400–1800 ml, typically
representing 30–35% of the patient’s blood vol
 Initiation of CPB inevitably leads to hemodilution by
the priming fluid
 Some degree of hemodilution is beneficial as blood
viscosity is reduced, improving microcirculatory flow
 Components – Blood prime or crystalloid/colloid prime
 Commonly used- ringers and normosol

51.  ADDITIVES- Heparin 1000–2500 U/l of prime to ensure
adequate anticoagulation
 Bicarbonate 25 mmol/l of prime as buffer
 Mannitol - Osmotic diuretic and free radical scavenger
 Calcium Needed if citrated blood is added to the
prime to prevent chelation of calcium
 Steroids To attenuate systemic inflammatory
response to CPB
 In children—blood—preferably CPD treated blood not
more than 7 days old is used –to increase the oxygen
carrying capacity

52. • As priming solution will be there in the circuit-when
blood enters –mixing &hemodilution occur—so
hematocrit decreases—the resultant hematocrit can be
calculated using the formula
• Hctr= Pts blood volume x preop Hct
-----------------------------------
pts blood volume+ CPB prime volume
OR
• Pts preop RBC volume/total volume of distribution at
start of CPB

53. PHYSIOLOGICAL EFFECTS OF
CPB
• Increases stress hormones (catecholamines , cortisol
,AVP)
• Decreased metabolism due to hypothermia + exclusion
of pulmonary circulation where these sub undergo
metabolism
• Variable SIRS—complement ,coagulation, kallikrein,
fibrinolytic system activation
• Blood contact with internal surface of CPB—acivates
alternate complement pathway[c3]+activates classical
pathway through Hageman factor.

55. • Mechanical trauma activates platelets &WBC—
production of oxygen derived free radicals- SIRS
• CPB alters & depletes glycoprotein receptors on
platelet surface—platelet dysfunction—increased
perioperative bleeding, potentiates coagulation
abnormalities.

56. METHODS TO DECREASE SIRS:
1. APROTININ THERAPY
2. LEUKOCYTE DEPLETED CARDIOPLEGIA
3. HEMOFILTRATION
4. LEUKOCYTE FILTER
5. FREE RADICAL SCAVENGERS
6. COX -2 INHIBITORS
7. PENTOXIPHYLLINE
8. SYSTEMIC CORTICOSTEROIDS –before &during
CPB

57. ALTERED PHARMACOKINETICS
IN CPB
• 1.Sudden increase in volume of distribution due to
hemodilution
• 2.Decreased protein binding
• 3.Changes in perfusion
• 4.Volume redistribution between central
&peripheral compartments
• 5.Alfa1 glycoprotein increases after CPB—affects
drug binding in post op period

58. END ORGAN EFFECTS OF CPB
• 1.Heart:
• Underlying mechanism –ischemia ; reperfusion.
• Factors causing ischemia during cpb—either increase O2
demand or decrease O2 supply
• 1.Abnormal perfusate composition
• 2.Persistent ventricular fibrillation
• 3.Inadequate myocardial perfusion

59.  4.Ventricular distention
 5.Ventricular collapse
 6.Coronary embolism
 7.Catecholamines
 8.Aortic cross clamping

60. • Myocardial cells may be irreversibly damaged ,
minimally damaged (stunned myocardium )
• stunned myocardium is susceptible to reperfusion
injury .
• Reperfusion can produce fol changes—structural—
myocardial edema, platelet deposition, neutrophil
activation, vascular injury& compression
• Biochemical—acidosis, decreased O2 use & high
energy Po4 production, increased catecholamines
&intracellular calcium , complement activation ,
increased free radicals
• Electrical— arrythmias
• Mechanical—impaired systolic/diastolic function
• Protection—proper cardioplegia

61. • 2.Brain:
• Cerebral microemboli , global cerebral hypoperfusion ,
cerebral hyperthermia , cerebral edema, BBB
dysfunction , drugs—causing post op cognitive decline
• 3.Kidney:
• Intravascular volume depletion , hypoperfusion can
lead to renal ischemia &ARF.
• 4.GIT:
Subclinical rise of liver enzymes & hyperamylesemia,
Gastroesophagitis , G.I hemorrhage , hyperbilirubinemia ,
hepatic &splenic & mesentric ischemia , intestinal
obstruction , infarction , perforation

62. • 5.Endocrines:
• Diabetes—aggressive control of perioperative glucose
during cardiac surgery –ideally—80-120mg%
• Risk of hyperglycemia—elderly, DM,CAD.
• Deleterious effects of hyperglycemia:
• 1.Decreased vasodilatation in response to ischemia
• 2.Decreased response to vasodilators
• 3.Decreased collateral coronary circulation
• 4.Increased free O2 radicals
• 5.Decrease in constitutive nitric oxide synthesis
• 6.Decreased ATP regulated activation of potassium
channels

63. ANAESTHETIC MANAGEMENT
Adults:-
Preinduction period:
 PREMEDICATION – in pts with CAD & good LV function—
heavy premedication , in frail pts—light premedication
 Benzodiazepine with/without opioid. Cautious sedation
in low CO , significant pul HTN
 If opioid is used half the dose of BZD is given
 To avoid hypoxia fol premed—5l /min o2 through nasal
cannula
 Continue all long term drugs esp beta blockers
.

64.  Elective surgery—stop aspirin 3-5 days before,
clopidogrel 5-7 days before ; but unstable angina we
may have to continue

65. • Preparation:
 Clear anesthetic plan
 Cockpit drill
 Keep drug infusions ready-one vasodilator; one inotrope
 2 large bore[>_16g ] I v cannula— drug infusions are
ideally given to central line
 Keep blood ready esp—redo cases as RV /GRAFT may
be adherent to sternum &may give away

66. MONITORING
• 1.BASIC MONITORS—Pulse oximetry, NIBP
• 2.ECG:--lead v5,II
• 3.Arterial BP
• 4.CVP & PA Catheterisation:
CVP—is in all pts , it is used to monitor CVP-guide fluid
management, provide portals for fluids , drugs , invasive
monitors
PAC: --not put for all pts—frail, complex op, EF<40—
50%,pul HTN, preference of surgical team.

68. • PAC may migrate distally during CPB—it may
spontaneously wedge without balloon inflation or
wedge with <1.5 ml air—if such a balloon is further
inflated—pul A rupture---fatal hemorrhage– so pull back
the PAC by 2-3 cm during CPB & inflate balloon slowly
• 5. In-line blood gas analysis and venous
saturation/hematocrit monitors
• 6. Non-invasive simultaneous arterial and venous
saturation monitors
• 7.Urine output
• 8.Temperature—sites : urinary bladder , rectal ,
esophageal , pulm artery , nasopharyngeal , tympanic,
direct myocardial , jugular bulb[reflects brain temp
accurately]

69.  9.LAB measurement:
 ABG-alfa stat—uncorrected values, adults on moderate
hypothermic CPB.
 pH stat—corrected values are used , used in children
 Combination—pH stat during cooling, alfa stat during
rewarming in pediatric CPB.
 Hct , serum potassium , ionised calcium , glucose, ACT

70. ACID BASE BALANCE
 Alpha- stat and ph-stat strategies for blood gas
management
 As blood temperature falls, gas solubility rises and the
partial pressure of carbon dioxide decreases (PCO 2
decreases 4.4% for every °C drop in temperature).
 With alpha-stat management, arterial gas samples are not
corrected for sample temperature and the resulting
alkalosis remains untreated during cooling
 Potential benefits in terms of the function of intracellular
enzyme systems and the advantage of preserving cerebral
autoregulation.

71.  In pH-stat management, arterial blood gas samples are
temperature corrected and carbon dioxide is added to
the gas inflow of the CPB circuit
 The PCO 2, and hence pH, is corrected to the same
levels as during normothermia.
 Results in cerebral vasodilation- advantages higher
levels of oxygen delivery to the brain and enhanced
distribution of blood flow.
 Higher cerebral blood flows associated with ph-stat
also have the potential to carry more gaseous or
particulate emboli to the brain

72. • 10.Surgical field:
 After opening sternum—lung expansion seen through
pleura , opening pericardium—RV is visible—cardiac
rhythm ,volume , contractility can be seen
 Blood loss & surgical manoeuvres must be closely
watched.
• 11.TEE:
 TEE provides information on new cardiac pathology in
12-39% cases leading to management changes in 5—
15%,causing no mortality,0.2% morbidity

73. • Applications of intra op TEE:
1.Assess ventricular function
2.Assess valvular function
3.Exam for residual cardiac air
4. Assess other cardiac structure
• 12.EEG– anesthetic depth
• 13.Transcranial doppler—for gas emboli

74. INDUCTION & MAINTENACE
• Cardiac surgeries can be done under
 GA +controlled ventilation
 High thoracic epidural+ GA [risk of
heparin hematoma]
 Only thoracic epidural

75.  SLOW,SMOOTH,CONTROLLED induction——small ,
incremental doses of selected agent +muscle relaxant as
soon as eyelid reflex is lost + controlled ventilation—to
avoid hypercarbia — HTN
 Intubation is done when anesthetic depth is reached or
arterial blood pressure is at lowest acceptable limits
 No single agent gives hemodynamic stability during
induction
 All anesthetic agents decrease blood pressure by
decreasing sympathetic tone ,decrease SVR, cause
bradycardia, direct myocardial depression

76.  Except etomidate[no effect on CO,HR]
 Ketamine—has sympathomimetic action—but may be
counterproductive in states of catecholamine depletion
 Volatile agents used as primary maintenance agent—
isoflurane , sevoflurane , desflurane—cause dose
dependent vasodilatation-decrease SVR , BP. They
induce preconditioning , mitigate reperfusion injury.
 Avoid—nitrous oxide—gaseous bubbles on rewarming
emboli

77. • 3 choices for anesthetic induction:
• A] High dose opioid anesthesia-eg— Sufentanil 15-
25ug/kg ; fentanyl—50-100ug/kg
• 1.Prolonged post op resp depression
• 2.Pt awareness during surgery[recall]
• 3.Fails to control hypertensive response to stimulation
in pts with good LV function
• 4.Rigidity during induction
• 5.Post op ileus
• 6.Impaired immunity

78. B] TIVA :-- Decreases cost of anesthesia –
 ETOMIDATE-0.2-0.6mg/kg over 30-60sec Maintainance
5-20mcrg/kg/min
 Propofol [0.5-1.5 mg/kg fol by 25—100ug/kg]
 Remifentanil—0.5-1ug/kg bolus fol by 0.25-1ug/kg
/min—short t1/2—so i.V morphine at end of operation
for post op analgesia

79. C] Mixed i.V /inhalational agents:
-Propofol[0.5-1.5mg/kg]; Etomidate[0.1-0.3
mg/kg]; Thiopentone[1-2 mg/kg];
Midazolam[0.05mg/kg]
--Isoflurane , sevoflurane, desflurane

80.  MAINTENANCE:
 Small dose opioid +VA
Nitrous oxide NOT used-expands intravascular bubbles.
 Fentanyl [1-3ug/kg/hr], sufentanyl[0.25-0.75ug/kg/hr],
remifentanyl[0.1-1ug/kg/hr]
 VA—isoflurane , sevoflurane , desflurane at 0.5-1.5 MAC
 OR low dose Propofol infusion [25-50ug/kg/min]

81. • Muscle relaxants— intubation, sternal retraction, dec
movt, shivering
• Rocuronium , vecuronium [if given with synthetic opioid
bradycardia], pipecuronium , doxacuronium ,
pancuronium [vagolytic- used for pt on beta blockers]
• Succinyl choline—acts on autonomic ganglia + cardiac
muscarinic receptors—so variable HR,BP. RSI
• Reversal— glycopyrrolate + neostigmine

82. • Hemodynamically compromised—ketamine[1-2mg/kg]
+midazolam[0.05-0.1mg/kg]—for induction
&maintenance
• --Good amnesia & analgesia with min post op
respiratory depression.
• Ketamine+diazepam also useful
• Fentanyl+midazolam also can be used

83. PRE CPB PERIOD
 1.ANTICOAGULATION
 2.CANNULATION OF THE HEART
 3.CAREFUL MONITORING—Pull back the
PAC by2-3cm , keep TEE in freeze mode
with scope in neutral/unlocked position
 4.MYOCARDIAL PROTECTION
 5.PREPARE FOR CPB—Pt position , drugs ,
head& neck examination
 Pre bypass check list

84. 1.ANTICOAGULATION
• Heparin:
• 1916- Jay Mc Lean
 Mast cells in lungs ,liver, pericapillary connective
tissue,around blood vessels
 Molecular weight ranging from 3 to 40 kda
 Commercially derived from bovine lung or porcine
intestinal mucosa.
 Onset is immediate
 half-life of approximately 2.5 hours at doses of 300–
400 USP units (U)/kg.

85.  MOA: Heparin simultaneously binds to AT3 &
thrombin.It has a unique pentasaccharide
sequence which binds to AT3.
 Heparin brings AT3 & thrombin closer
 AT3 inhibits procoagulant effect of thrombin by
binding to active serine residue of thrombin.
 The inhibitory effect of AT 3 is increased by 1000
fold.
 It also affects factor Xa

86. • Dosing in cpb:
• BULL & co—1975—dose according to ACT.
• ACT [activated clotting time]—baseline ACT is
measured[80-120sec].
• Heparin –300-400 U/kg as i v bolus. Subsequent heparin
dose is adjusted so as to reach a ACT OF 480 sec [min
400 sec].

87. CLINICAL FACTORS affecting ACT:
• Hemodilution Prolongs the ACT in the presence of
heparin
• Hypothermia Prolongs the ACT
• Thrombocytopenia Prolongs the ACT
• Platelet inhibitors Prolongs the ACT
• Low fibrinogen levels prolongs the ACT
• Platelet lysis Shortens the ACT
• Aprotinin Prolongs the ACT with celite activator
• Surgical stress Shortens the ACT

88.  ACT is not a monitor of heparin efficacy.
 Heparin assay must be done.
 Other tests-
1. Point of care [POC ]monitors
2. HepCON HMS system]—uses protamine
titration assay to calculate heparin
concentration
3. HiTT[high dose thrombin time]-more
specific test of heparin effects on
thrombin, correlates well with heparin
concentration before &during CPB &less
artifacts.

89. UNIQUE CONSIDERATIONS
 1.AT3 DEFICIENCY/HEPARIN RESISTANCE:
• Def: defined as failure to raise the ACT to expected levels
despite an adequate dose and plasma concentration of
heparin
• ACT<480sec after 500u/kg heparin given I.V or ACT<400
sec at any time during CPB &heparin administration.
• CAUSES- 1. congenital or acquired AT-III deficiency
• 2. Prior treatment with heparin causes depletion or
dysfunction of AT-III
• 3. presence of large quantities of heparin-binding protein
in the circulation, which binds to and inactivates heparin
• Rx : supplemental heparin 600-800U/kg.
if refractory—FFP,AT3,recombinant AT3.

90.  2.HEPARIN REBOUND:
• Def: Bleeding occuring 1 hour after protamine
neutralisation
• -Indicates residual heparinisation
• Causes:1.Slow dissociation of protein bound heparin
after protamine clearance
• 2.More rapid clearance of protamine than heparin
• 3.Lymphatic return of extracellular sequestered
heparin
• 4.Clearance of an unknown heparin antagonist
• Treatment:supplemental protamine

91.  3.HEPARIN INDUCED THROMBOCYTOPENIA
• Incidence—20-50% after CPB,prevalence—1-3%
• Def : immune mediated prothrombotic disorder seen in
pts exposed to heparin.
• Pathogenesis: it is due to antibodies against Platelet
Factor4 and heparin complex
• The Pf4-heparin complex binds to platelets leading to
immune mediated platelet activation

92.  Clinically platelet count < 1 lac/mm3 or < 50% of
baseline.
 It is the strength of pf4 –heparin immune response &
not antibodies which determine hit.
 Types— Type1-platelet>1 lac
Type2-platelet<1 lac +thrombosis
ACUTE HIT: documented thrombocytopenia + detectable
Ab with/without thrombosis
 delaying surgery, if possible, until HIT antibodies are
negative
 Use alternative anticoagulant - bivalrudin or hirudin
 Combinations of Uf. heparin and antiplatelet agents
such as epoprostenol or tirofiban

93.  SUBACUTE HIT: Recently diagnosed HIT +resolution of
tcp+ hit ab titres still positive
• Defer surgery
• If mandatory use bivalirudin
 PRIOR HIT:[prior diagnosis of HIT + Ab not detectable]
• Heparin can be used ,but not long term , reverse
heparin completely

94.  ALTERNATIVES TO HEPARIN
1. Low-molecular-weight heparin (LMWH
2. Danaparoid - 30% cross-reactivity with heparin
antibodies
3. Fibrinolytics- Ancrod is a defibrinogenating agent
extracted from Malayan pit viper venom. No antidote
4. DTIs- These directly inhibit the procoagulant and
prothrombotic actions of thrombin and do not require a
cofactor.
Their advantage is that they do not interact with or
produce heparin-dependent antibodies
Eg: Lepirudin, Agatroban , Bivalirudin

95. CANNULATION
 ARTERIAL CANNULA: preferred site—
ascending aorta.
 It is easily accessible , additional incision is
not needed , larger cannula —so greater
flow , decreased risk of dissection as
compared to femoral/iliac
 Complications—arterial dissection,
hemorrhage & hypertension , cannulation
may be in aortic arch ,emboli—plaque/air in
&around the cannula , dysrrhythmias.
 This is always inserted first

97.  SIGNS OF CANNULA MALPOSITION:
1. U/L blanching of face ,
2. U/L decreased carotid pulse
3. BP asymmetry in both arms
 CONTRAINDICATIONS FOR ASC aorta—atherosclerosis
,aneurysm ,dissection ,cystic medial necrosis—so use
alternative sites-femoral
• Prior to placing—1.SBP-90-100 as hypertension
increases risk of dissection
• 2.De-air cannula totally
• 3.Demonstrate back flow of blood into arterial line
before starting CPB

99. VENOUS CANNULA
• SINGLE cannula:- inserted into RA & directed
inferiorly—drainage holes in IVC &RA,SVC &CORONARY
sinus
 Adv : simple , fast , only one incision
 Disadv : when heart is lifted drainage may be affected
especially if its in RA

100.  BICAVAL/TWO STAGE CANNULA : both SVC,IVC are
cannulated.
 Loops placed around vessels which are tightened to divert
all caval blood away from heart
 Disadv : blood in RA via coronary sinus is not drained ;
 Large cannula obstruction—svc—sudden [ face , neck
swelling ]; IVC—INSIDUOUS as decreased venous return—
decreased filling pressures
 Complications : hypotension due to impaired ventricular
filling ; arrhythmias—usually—atrial , PSVT

102. CARDIOPLEGIA
 A still heart is needed for surgery
 Heart can be arrested in diastole/VF
 PRIOR TO CARDIOPLEGIC use , asc aorta cross clamping
proximal to cannula was used to arrest heart in VF
along with hypothermia . But,only short ischemic
times could be achieved[10 min]—if prolonged
resulted in severe , persistent myocardial dysfunction.
 Cardioplegic solution with potassium used to arrest
heart in diastole—provide longer ischemic time—
produce electromechanical arrest for surgery

103. MYOCARDIAL PRESERVATION
 Four concepts:
 1.Protection begins before arrest[ treat
dehydration , hypoglycemia]
 2.Decrease metabolic requirements during
arrest[by systemic hypothermia]
 3.A favorable metabolic milieu must be
there always to provide safety if arrest
happens
 4.Reperfusion modification must be done if
ischemic insult happens

104. GOALS OF CARDIOPLEGIA:
1.Quiet bloodless field
2.Limit myocardial damage by decreasing
intracellular acidosis , edema , depletion of
ATP stores
3.Preserve coronary endothelial function &
myocardial flow
4.Reduced injury during reperfusion

105.  STRATEGIES for delivering cardioplegia:
 Antegrade: Into aortic root—but may not
reach myocardium supplied by blocked
artery
 Retrograde: Into coronary sinus ; delivery
to RV myocardium is difficult—posterior
interventricular vein[RV]—enters coronary
sinus close to its entry into RA –the
cannula is usually beyond vein
 Both - antegrade+retrograde

106.  Cold - <10`c with use of heat exchanger—decreases
oxygen demand
 Warm - 37`c—reduce reperfusion injury , preserved
coronary endothelial function , rapid reestablishment
of myocardial energy stores , reduced calcium influx ,
less activation of wbc , platelets , upregulates
protective heat shock proteins
 Single hot shots –at initiation &termination of CPB –
restores ATP levels—decreases subsequent injury---final
hot shot can be enriched with aa-glutamate,aspartate—
to replenish TCA intermediates

107. • MECHANISM: Cardioplegia — increased extracellular
potassium — decreases transmembrane potential 
interferes with normal sodium current during
depolarization —decreases rate of rise , amplitude ,
conduction velocity of subsequent action potential —
sodium channels are completely inactivated  action
potentials are not established  heart arrested in
DIASTOLE

108.  CONTENT-
 Blood containing or crystalloid cardioplegia
• Potassium- diatolic arrest
• Sodium- reduces intracellular edema
• Chloride ions maintain the electroneutrality of the
solution
• Calcium- prevent influx of Ca2+ during reperfusion
• CPD- to limit calcium infl ux during ischemia
• (tris-hydroxymethyl aminomethane, THAM)- buffer
that prevents acidosis
• glutamate and aspartate, glucose
• Mannitol – reduces oedema

109.  Cold cardioplegic mixture containing high-dose potassium
(20 meq/l) infused antegrade into the aortic root at a
flow rate of 300 ml/minute for 2 minutes, followed by
retrograde coronary sinus infusion at a flow rate of 200
ml/minute for 2 min
 “Maintenance” low-dose cold potassium (8–10 meq/l)
blood cardioplegia is infused at a flow rate of 200
ml/minute for 1 minute
 Last distal anastomosis is completed - the “hot shot” of
warm substrate-enhanced cardioplegia is delivered, first
antegrade & then retrograde
 Body and cardioplegia are re-warmed
 the cardioplegia is washed out of the myocardium by
retrograde infusion of plain warm blood at a fl ow of 300
ml/minute.

110.  Blood cardioplegia: source of oxygen, buffer,
antioxidant—continuous—low flow
 Intermittent –at 20 min interval ,few hundred ml—
1litre given
 Crystalloid cardioplegia:
• Potassium[10-40 meq/l] - if >40 meq/l — paradoxic
increase in energy need ; sodium<140meq/L –as
ischemia increases intracellular sodium
• Calcium—0.7—1.2mmol/l — maintains cell integrity
— calcium free solutions are never used – as they
lead to massive influx of calcium into the
myocardial cells on reperfusion--`calcium
PARADOX`;
• Magnesium —1.5-15 mmol/L –controls excess
intracellular influx of calcium

112. SYSTEMIC HYPOTHERMIA
 After initiating CPB—INTENTIONAL HYPOTHERMIA [core body
temp=20-32`c],for 10`c fall 50% decrease in metabolic
requirement
 Following anticoagulation CPB is instituted with a constant
fl ow rate of 2.4 l/minute/m 2 and cooling immediately
commenced with a water bath to a blood temperature
gradient of <10°C
 Vasoconstrictors (e.g., phenylephrine) or vasodilators (e.g.,
glyceryl trinitrate, nitroprusside) are used to ensure a mean
arterial pressure of 50–60 mmHg
 Cooling continues until brain (e.g., nasopharyngeal) and
core body (e.g., bladder) tem- peratures have equilibrated
at the target temperature for 10–15 minutes.
 .

113.  continuous monitoring of the EEG, evoked potentials or
jugular venous saturation is used as a guide to the
adequacy of cerebral cooling
 At end of operation—rewarm by heat exchanger—
restores normal body temperature
 Profound hypothermia—15-18c –total circulatory arrest

114.  POSITIONING –to avoid pressure related
injuries—as soft tissue injury will be
increased by hypothermia & decreased
perfusion during CPB.
 Proper arm position,head padded,eyes
lubricated &padded
 All major drugs are kept ready

115. INITIATION OF CPB
After cannulas are secured , ACT is acceptable ,
perfusionist is ready  CPB is initiated  clamps placed
across cannulas are removed first  venous then arterial
 main CPB pump is started  reservoir level gradually
increases & CPB flow is gradually increased  if venous
return is low  pump prime can empty  air can enter
 in such cases check for cannula placement , forgotten
clamps ,kinks , air lock; slow down pump flow till
problem is solved  add volume to
reservoir[blood/colloid]  with full CPB heart must
gradually empty  if not , look for mal positioned
venous cannula , AR

116.  Cannulas are secured
 ACT is acceptable
 Perfusionist is ready
 CPB is initiated
 Clamps placed across cannulas are removed first

117.  Venous then arterial
Main CPB pump is started
 Reservoir level gradually increases & CPB flow is
gradually increased
 If venous return is low pump prime can empty air
can enter
 Add volume to reservoir[blood/colloid]
 With full CPB heart must gradually empty

118.  Pump flow is gradually increased to 2-
2.5L/MIN/M2
systemic arterial pressure is monitored
radial artery pressure is 30-40 mm hg
abrupt hemodilution
decreases blood viscosity &decreased SVR

119. • If persistent SBP <30mm hg
• 1.Search for aortic dissection
stop CPB recannulate aorta distally
• 2.Poor venous return
• 3.Pump malfunction
• 4.Pressure transducer error

120. • Mean arterial pressure = pump flow x SVR
• Manipulate pump flow &SVR in CPB—to
maintain MAP &blood flow
• Adequate—MAP —50-80 mm hg , blood
flow=2-2.5L/min/m2 or 50-60 ml/kg/min
these depend on core body temperature
• If MAP >100REDUCE pump flow or add
isoflurane to oxygenator inflow gas  still
MAP >100 add sodium nitroprusside

121. • Ventilation:
• Continue ventilation till adequate pump flows are
reached & heart stops pumping blood
• Even after full CPB ventricular ejection continues
briefly until LV volume reaches a critical level
• If ventilation is discontinued prematurely—then
pulmonary blood may act as a R-L shunt  hypoxia
• Some people continue to ventilate with low flows [1-
2l/min] with small peep[5 cm h2o] to prevent post op
pulmonary dysfunction

122. TERMINATION &WEANING
FROM CPB
• STEPS involved in discontinuing CPB:
• 1. Rewarming must be completed
• 2. Air must be evacuated from heart
&bypass grafts—by surgical maneuvres
• 3. Aortic cross clamp must be removed
• 4. Lung ventilation must be resumed

123. GENERAL GUIDELINES FOR
SEPERATION FROM CPB
 1.Core body temp=not more than 37`c
 2.Stable rhythm—preferably sinus
 3.ADEQUATE HR—80—100 bpm,fast HR is
preferable than slow
 4.Lab parameters needing treatment:
 -Ph<7.2;hct<22%
 5.Adequate ventilation with 100% oxygen
 6.All monitors must be working

124. REWARMING
 Core temperature above 36 deg C is the first step in
weaning from CPB.
 Multiple temperature monitoring sites on blood
temperature and the temperature of the heat exchanger
 Body temperature may be monitored at a number of
sites, for example nasopharyngeal, esophageal,
intracardiac, bladder or rectum
 Re-warming is not uniform A combination of bladder
temperature and the temperature of the venous blood
returning to the bypass circuit

125.  If re-warming is inadequate, or if the core-surface gradient is
greater than 7 deg unwanted increase in oxygen
consumption./
 Core temperature should not be allowed to rise > 37 deg as
this will lead to tachycardia and may increase the risk of cns
dysfunction
 Patient should be re-warmed using the arterial blood temp
(37.5 and 38°C) & patient core temperature as guides to the
rate and extent of re-warming
 Temp bt the water temperature in the heater–chiller unit and
the arterial blood < 10°
 Re-warming the patient to 37°C (nasopharyngeal) is usually a
max
 The rate of re-warming should allow time for distribution of
heat between core and peripheral tissues, (using vasodilators
to enhance peripheral blood flow and thus heat distribution)

126. ELECTROLYTES AND ACID BASE
BALANCE
 Electrolyte abnormalities should be corrected before
separation from CPB in order to optimize myocyte
function.
 In particular, potassium, magnesium and calcium should
be kept within the normal range
 Good glycemic control be achieved
 Metabolic acidosis to be treated

127. HEMOGLOBIN
 The Hb concentration should be >7.5 g/dl prior to
termination of CPB.
 In situations where myocardial oxygen supply or whole
body oxygen delivery are expected to be impaired post-
cpb - aim for a higher Hb conc
 When bleeding is expected to be an ongoing problem
in the post-cpb period higher Hb aimed.
 Coexisting respiratory disease, congenital heart disease
who remain cyanosed after surgery, a higher Hb
concentration is mandatory.
 Stored, concentrated RBC should be immediately
accessible for use in the post- bypass period.

128. COAGULATION
 Due to the nature of cardiac surgery, particularly the
anticoagulation required and the effects of the
extracorporeal circuit on the clotting cascade and
platelet function, patients under- going CPB are at signifi
cant risk of bleeding.
 Consequently, ready access to serum clotting factors and
platelets must be ensured.
 Following separation from CPB and reversal of anti-
coagulation, assessment of clotting and platelet function
should be performed
 Persistent surgical bleeding and the absence of visible
clot for- mation should initiate blood product support

129. VASOACTIVE SUPPORT
 VOLUME-- in addition to ready access to blood
products, colloid and crystalloid solutions should be
immediately available to increase circulating
volume
 Vasoactive drugs vasopressors, inotropes and
vasodilators must be available immediately
 To be based on the patient’s circulation, nature of
the surgery and local team protocols

130. ANESTHESIA
 Anesthesia, analgesia and neuromuscular
blockade must be assessed and
supplemented as required
 Weaning from CPB may instigate either a
change in anesthetic technique (e.g.,
intravenous to volatile) or an adjustment
to dose delivery.
 Anesthesia is properly maintained and this
should be confirmed by the team
members

131. CARDIAC FUNCTION
 Assessment should concentrate on three main areas:
rate, rhythm and contractility.
 The ventricles are less compliant & will not inc stroke vol
 HR- 80 and 100 bpm
 Stiff ventricle - increase contribution of atrial
contraction to stroke volume - sinus rhythm is always
preferable if possible.
 Epicardial pacing leads and an external pacemaker should
always be immediately
 Contractility can be assessed by direct visualization of the
right ventricle. If in use, trans- esophageal
echocardiography (TOE) enables a more detailed
examination of all four chambers.

132. EVENTS IMMEDIATELY PRIOR
TO INITIATING WEANING
 Mechanical ventilation During CPB the lungs are
allowed to deflate fully or to remain slightly inflated at
low levels of (PEEP)- alveolar collapse
 Prior to weaning from CPB full and effective expansion
of the lungs should be ensured with manual
hyperinflation
 Once expansion is achieved, mechanical ventilation is
resumed, usually with PEEP
 Ventilation should be initiated when there are signs of
1. significant LV ejection 3.competent aortic valve
2. cardiac ejection 4. non interfering

133. DE-AIRING OF THE HEART
 Air in right-sided chambers is innocuous as long as its
volume is not enough to prevent forward flow
 Air in the left side is dangerous
1. cerebral air embolus with postoperative morbidity
2. coronary air embolus, which may cause transient
regional ventricular dysfunction
 Direct cardiac massage
 syringing of left -sided chambers
 venting of the aorta or left -sided chambers in a head
down position, prior to, and after, aortic unclamping.
 ventilate the lungs during the de-airing process to
displace air that accumulates in the pulmonary veins.

135. SEQUENCE OF EVENTS PRIOR TO
WEANING FROM CPB
1. Confirm effective ventilation
2. Re-enable physiological alarms
3. Final check of electrolytes and acid–base
status Correct acidosis if required
4. Effective de-airing of heart
5. Confirm satisfactory pacing lead thresholds
6. Confirm vasoactive agent delivery
7. Engage all team members

136.  Re-establish ventilation  clamp venous line to
gradually decrease venous return to reservoir 
increase the intravascular volume by continued inflow
via arterial cannula-lower the pump flow into
aorta— i.e PARTIAL CPB state—now some venous blood
is going to reservoir ,some into RV
 LUNGS-when optimal loading conditions & optimal
contractility is reached  CLAMP aortic inflow line-
remove all cannulas REVERSE HEPARIN

137. HEPARIN REVERSAL BY
PROTAMINE
• Protamine is a positively charged protein which binds
& inactivates heparin. The heparin—protamine
complex is then removed by reticuloendothelial
system.
• Dose of protamine:--
• 1.1-1.3 mg protamine for every 100u heparin given
initially—until desired ACT is got
• Automated heparin-protamine titration assays which
measure residual heparin concentration—so the
protamine dose
• Excess protamine may itself act as an anticoagulant
having 1/100th action of heparin

138. PROTAMINE REACTION
• 1.Isolated hypotension
• 2.Hypotension with bronchoconstriction with increased
PAP,acute RVF
• EXPLANATION: mast cell degranulation, endothelial release
of nitric oxide, and hypotension associated with rapid
infusion.
• Anaphylactoid reactions include protamine sensitivity
reactions- allergic in nature - are mediated by IgE antibody
• nonimmunologic mechanisms, which may involve IgG
antibodies or complement activation
• Risk factors— pt on neutral protamine hagedorn (NPH)
insulin ,fish allergy, history of other allergies
• --Possible risk factors—prior protamine exposure,decreased LV
function,hemodynamic instability

139. TREATMENT OF PROTAMINE
REACTION
 1.Give protamine slowly>5 min
 2.If h/o documented protamine allergy—
opcab,non HEPARIN cpb,non protamine
reversal of heparin—pf4,heparinase.
 3.If hypotension—its treatment
 4.If severe reaction return to CPB MUST
BE CONSIDERED

140. • BLEEDING PROPHYLAXIS:- antifibrinolytic agents-
aprotinin , tranexamic acid , EACA
• Indications:
1.Repeat operations
•
2.Pt who refuse blood products[jehovahs witnesses]
•
3.Pt on GP iib/iiia inhibitors—high risk for post op
bleeding—abciximab[24-48hr],eptifibatide[2-
4hr],tirofiban[4-8 hr]
•
4.Preexisting coagulopathy
•
5.Long,complicated cardiac operations

141.  APROTININ:-
 Inhibits serine proteases—plasmin,kallikrein,trypsin
 Preserves platelet function—adhesion,aggregation
 Blunts inflammatory response associated with CPB
 ADVERSE EFFECT—anaphylaxis on repeat exposure
 A test dose[1.4 mg]is given prior to loading dose of 280
mg which is added to CPB prim

142.  Epsilon amino caproic acid[5-10g fol by
1g/hr]
 Tranexamic acid-10mg/kg fol by
1mg/kg/hr
 Advantages:do not affect ACT,less allergic
reaction
 Disadvantages:do not preserve platelet
function—preoperative collection of
platelet rich plasma by pheresis fol by
post op transfusion

143. LUNG
 Atelectasis,
 Bronchospasm ,
 Hemothorax,
 Pneumothorax,
 Pulmonary edema,
 Blood clots/mucous plugs in ET tube,
 Post perfusion lung syndrome

144. POSTOP PERIOD
 Most pts are on mechanical ventilators for 2—12hrs
 Sedation with small doses of morphine[2-3mg] or
propofol infusion[20-30 ug/kg/min]
 If chest tube drain shows >10ml/kg/hr in absence of
hemostatic defect ongoing bleedreopen
immediately.

145. PERSISTENT BLEEDING
 Causes—
1.Inadequate control of bleeding sites
2.Inadequate heparin reversal
3.Reheparinisation
4.Thrombocytopeni
5.Platelet dysfunction
6.Hypothermia—accentuates the hemostatic
defects
7.Undiagnosed hemostatic defects
8.Heparin rebound

146. MEASURES TO REDUCE
BLEEDING
 Antifibrinolytic agents – EACA, tranexamic acid
 Aprotinin, a serine protease inhibitor
 Heparin and protamine dosing: ACT should return to
baseline following administration of protamine;
additional doses of protamine (25–50 mg) may be
necessary
 Desmopressin is an analogue of vasopressin that
releases VWF from normal endothelial cells

147. MYOCARDIAL PROTECTION
1. N.O supplemented Cardioplegia
2. LV Vent
3. Ischemic preconditioning
4. Leucocyte filters
5. Hypothermia

149. CEREBRAL PROTECTION
 Avoid hemodynamic compromise during induction
 During aortic cannulation, less calcific areas should be
cannulated
 Avoid hypercarbia
 N2O avoided
 Use of membrane oxygenator
 Maintainence of MAP 50 mmHg ( 20-30mmhg-
hypothermia, 60-130 during normothermia)
 Alpha stat management of pH
 Arterial line filters
 Avoid hyperthermia during CPB and rewarming
 Pharmacological therapy- free radical scavengers,
propofol, thiopentone,aprotinin

151. CPB in pediatric cardiac
operations
 Differences between adult &pediatric cpb
 Parameter adult pediatric
 1.Hypothermia 25—30c 15-20`c
 2.Total circulatory
arrest rare common
 3.Pump prime
Dilution effect on 25-33% 150-300%
Blood volume
 Additional additives -- blood,albumin

152.  4.perfusion pressure 50-80mm hg 20-50mm hg
 5.alfa stat + --
 6.pH stat - +
 7.measured PaCO2 30-45mm hg 20-50mm hg
difference
8.GLUCOSE REGULATION
-hypoglycemia rare common-low
hepatic glycogen
-hyperglycemia common rebound
hypoglcemia

153. QUESTION BANK
 Long essay
1. Describe the currently available methods of myocardial protection
during coronary bypass grafting
 Short essay:
1. Protamine sulphate- 2005 sept
2. Hypothermia -2011 nov
3. ACT-2007 nov
4. Heparin 2008 may
5. Discuss the problems associated with an adult pt undergoing ASD
closure in cardiology procedure room- 2014 may
6. Cardioplegia – may2011
7. Cerebral protection – nov 2012

154. REFERENCES
1.WYLIE- 5 TH EDITION
2.MILLER’S ANAESTHESIA —7 TH EDITION
3.CLINICAL ANESTHESIOLOGY-MORGAN&
MIKHAIL—4TH EDITION
4.KAPLAN’S CARDIAC ANESTHESIA- THE ECHO
ERA—6TH EDITION
5.CPB- PRINCIPLES AND PRACTICE -GRAVLEE—
1ST EDITION

156. REFERENCES