Physiology of CPB, working principle of bypass machine, parts of bypass machine, cardioplegia,temperature and cpb, cpb in gravid patients

1. J J M MEDICAL COLLEGE
DEPARTMENT OF ANAESTHESIOLOGY
PHYSIOLOGY OF
CARDIOPULMONARY BYPASS
PRESENTATION BY MODERATOR
DR. KSHAMA BALAKRISHNA DR. ABDUL SHABEER
1

2. INTRODUCTION
Cardiopulmonary bypass is a form of extracorporeal circulation which
provides circulatory and respiratory support along with temperature
management to facilitate surgery on heart and great vessels.
• Patient’s blood is rerouted outside the vascular system and the
function of heart, lungs and to a lesser extent, kidneys is
temporarily assumed by a surrogate technology
• Provides motionless, bloodless surgical field
2

3. HISTORICAL ASPECTS
• April 5, 1951- Dr. Clarence Dennis led the team performing the first
known operation involving open cardiotomy with temporary
mechanical takeover of both heart and lung functions in University of
Minnesota Hospital.
• May 6, 1953- first successful human cardiac surgery using CPB
Dr. John Gibbon at Thomas Jefferson University Hospital in
Philadelphia .They repaired an atrial septal defect on an 18 year old
woman. The heart-lung machine used by Gibbon was later developed
by John W. Kirklin at Mayo Clinic.
3

4. HISTORICAL ASPECTS
• The oxygenator was first conceptualised by Robert Hooke in the 17th
century and developed into practical extracorporeal oxygenators by
French and German experimental physiologists in the 19th century.
• 1983- Ken Litzie patented a closed emergency heart bypass system
which reduced circuit and component complexity and improved
patient survival after cardiac arrest as it could be deployed in non-
surgical settings.
4

5. INDICATIONS
• Coronary Artery Bypass Graft (CABG)
• Congenital Heart Diseases – repair of congenital heart defects (ASD,
VSD, AVSD), palliation of congenital heart defects (TOF, TGA)
• Transplantation – cardiac, lung, heart-lung transplantation
• Heart Valve Repair and Replacement – AS, AR, MS, MR
• Repair of large aneurysms (aortic aneurysms, cerebral aneurysms)
• Pulmonary thrombectomy, pulmonary thromboendarterectomy
5

6. GOALS OF CPB
Oxygenation and carbon dioxide elimination
Circulation of blood
Systemic cooling and rewarming
Diversion of blood from heart to provide bloodless surgical field
6

7. THE CPB CIRCUIT
• Tubing
• Cannulae
• Reservoir
• Pump
• Oxygenator
• Cardioplegia system
• Suction and vent pump
7

8. TUBING
• Connect various components of the CPB machine- conduct blood
in and out of patient’s vascular system
• Material – PVC, acceptable haemolysis rate and durability
• Surface coated PVC used- better biocompatibility
• Surface coatings- covalently bonded heparin; newer-
poly2methoxyethylacrylate, phosphorylcholine, trillium
• Plasticisers can leach from the tubing into blood
8

9. CANNULAE
• Connect patient to heart-lung machine
• Wire reinforced- avoid kinking, PVC material
• 2 key steps before bypass- anticoagulation and
vascular cannulation
9
Goal of vascular cannulation
Provide access whereby the CPB pump may divert all systemic venous blood
to the pump oxygenator at the lowest possible venous pressures and deliver
oxygenated blood to the arterial circulation at pressure and flow sufficient to
maintain systemic homeostasis.

10. ARTERIAL CANNULATION
• Preferred site- ascending aorta (3-4cm distal to aortic root); alternate
sites- femoral artery, axillary artery, LV apex
• Arterial cannulation done before venous cannulation
• MAP <80, SBP<90-100mm of Hg is desired during aortic cannulation
• Alternate site cannulation preferred- severe aortic atherosclerosis, aortic
aneurysm or dissection, redo procedures
• Complications- embolization of air or atheromatous debris, inadvertent
cannulation of aortic arch vessels, aortic dissection and other vessel wall
injury
Anaesthetic concerns- unilateral blanching of face, unilateral diminution of
carotid pulse, new asymmetries in BP can mean cannula malposition.
10

11. A: Metal-tipped right-angled cannula with plastic moulded flange
B: Similar design but with a plastic right angle tip and moulded flange
C: Diffusion-tipped angled cannula designed to direct systemic
flow in four directions to avoid a "jetting effect"
D: Integral cannula connector and luer port (for de-airing) incorporated into some arterial cannulas.
11

12. VENOUS CANNULATION
• Allows deoxygenated blood to be drained from the patient into CPB
• Bicaval cannula- inserted into SVC and IVC joined by Y-piece, open heart
surgeries requiring right atrial access (additional vent or atriotomy is
needed to drain blood from coronary sinus.)
• Single atrial cannula- inserted into RA, closed heart surgeries
• Cavoatrial cannula- inserted into RA and narrower tip in IVC
• Alternate sites- femoral vein(minimally invasive or redo procedures); long
cannula inserted upto RA (TEE assisted)
Anaesthetic concerns- Hypotension, arrhythmias; SVC obstruction presents
as head and neck venous engorgement, conjunctival oedema and elevated
SVC pressure. 12

13. BICAVAL CANNULA
CAVOATRIAL CANNULA
VENOUS CANNULA
13

14. RESERVOIR
• Collects the blood drained from the heart
• Venous drainage occurs through gravity or vacuum assisted
• The amount of venous drainage depends on:
1. CVP
2. (Height of the table - the top of the blood level in the venous reservoir)
3. Resistance in the venous cannulas, venous line and connectors, and
venous clamp, if one is in use
• Reservoir pressure>60mm of Hg  increase micro bubble count in arterial
infusion lines
• Excessive drainage  "chattering" or "fluttering” of venous cannula 14

15. OPEN RESERVOIR
• Hard shelled
• Passive removal of entrained venous air
• Integral +/- pressure release valve for
vacuum application
• Cardiotomy & defoaming circuit
• Fluid level in reservoir- critical; if allowed
to empty can cause air embolism
CLOSED RESERVOIR
• Collapsible plastic bags
• Eliminate gas-blood interface; reduced
risk of air embolism
• Require separate circuit for salvage of
suctioned blood
• Less contact with artificial surface-
decreased inflammatory activation, better
sterility, reduced need for postop
transfusion
15

16. PUMP
• Constant blood flow is delivered to the patient by a mechanical pump.
• An ideal pump is based on the Hagen- Poiseuille formula:
• It must be able to generate blood flow and pressure against a degree of resistance
• Low index of haemolysis (plasma Hb/100ml of pumped blood)
• Biocompatible material and create no areas stasis or turbulence; able to adjust to
different sizes of extracorporeal tubing
• Have low priming volumes and easily controllable
• In the event of a power failure, the pump should be manually operable
Blood flow rate = (pressure gradient)x (tube radius)4x p
(fluid viscosity)x (tube length)x 8
Pressure
Resistance
=
16

17. ROLLER PUMP
• Types- single roller (obsolete), double roller
(most commonly used), multi roller (clinically
unavailable)
• Length of a PVC/silicone rubber/ latex rubber
tubing situated against a curved raceway which is
compressed by two rollers located on the ends of
rotating arms at 180o to each other
• Positive displacement pump
• Blood flow depends on ID of tube, rpm and
diameter of the pump head
• Haemolysis and spallation from tubing
17

18. CENTRIFUGAL PUMP
• Vaned impeller/ stacked cones within a plastic
casing are magnetically coupled at the base with
an electric motor
• When rotated rapidly, centrifugal force is
generated blood is propelled forward
• Afterload dependent
• CF = mass of blood x radius of pump head x speed
of revolutions (rpm)
• Non-occlusive pumps  prevent generation of excessive pressure in the circuit
avoiding circuit rupture
• Improve platelet preservation, renal function, neurological outcomes; can be
used for long procedures
18

19. ROLLER PUMP CENTRIFUGAL PUMP
Afterload independent Afterload dependent
No flowmeter required Needs flowmeter
Increase blood trauma and tubing
debris
Decrease blood trauma and tubing debris
No backflow occurs Retrograde flow possible if pump stops
Cheap Expensive
Short-term use Long-term use
Bulky Portable
Circuit disruption from excessive line
pressure
No disruption
Greater risk of air embolism Lesser risk of air embolism
Priming volume less Priming volume more
19

20. OXYGENATOR
• Substitutes patient’s native lungs
• Types of blood oxygenators
1. Bubble oxygenators- bubbling oxygen through blood
2. Disc oxygenators- exposing a blood film to oxygen rich atmosphere
3. Membrane oxygenators- sheet oxygenators and hollow fibre oxygenators
• Native lung and the oxygenator
1. Both have a gas space and a blood space separated by a membrane
2. Both are driven by passive diffusion gradients 20

21. MICROPOROUS MEMBRANE OXYGENATORS
• Microporous polypropylene material
• Thin straws with an OD of 200-400μm, wall thickness of
20-50μm, and TSA of 2-4 m2
• Priming volume 135-340 mL; arterialize up to 7L/min of
venous blood
• Gas space (inside the straws)- continuous “sweep” of gas
• Blood space (outside the straws)
• Gas inlet and outlet ports; Gas exchange- driven by pressure gradient. Volatile
anaesthetics can be delivered
• Microscopic (0.5-1.0μm)- prevent plasma, allow gas to pass through
• Multiple gas outlet ports to depressurize the gas space – avoid gas embolism 21

22. CARDIOPLEGIA SYSTEM
• Myocardial protection and motionless surgical field
• Arrest in diastole by administration of cold K+
enriched cardioplegia solution
• Interruption of myocardial electromechanical activity
and metabolism
• Myocardial O2 consumption by 97%; allows
interruption of blood flow for 20- 40min
• Antegrade, Retrograde and Ostial cardioplegia

22

23. Cardioplegia solution
1. K+ enriched whole blood
2. K+ enriched solution - whole blood
to crystalloid (4:1 or 8:1)
• 1000- 1500mL high-K mixture (20-
30mEq)- initiation;
• 200- 500mL low-K mixture
(10mEq) maintenance
23
St Thomas cardioplegia solution
Na+ 110 mmol/L
K+ 16 mmol/L
Mg2+ 16 mmol/L
Ca2+ 1.2 mmol/L
NaHCO3
- 10 mmol/L
Del Nido cardioplegia solution
Mannitol 20%, 16.3mL, 3.26mg
Magnesium sulphate 50%, 4mL, 2g
Sodium bicarbonate 8.4%, 13mL, 13mEq
Lidocaine 1%, 13mL, 130mg
Potassium Chloride (2mEq/mL) 13mL, 26mEq

24. SUCTION AND VENT PUMP
• LV venting- decompression and de-airing
• Reduces myocardial rewarming, prevents ejection of air,
facilitates surgical exposure, myocardial preservation
• Sources of blood returning to LV- bronchial (1% of CO)
and thebesian veins ;
• abnormal sources- persistent left SVC, PDA, ASDs, VSDs, AR
• Aortic vents- same cannulas that deliver antegrade cardioplegia
• Direct LV vents
• All vents attached to suction (roller pump/ siphon) and blood is returned to
cardiotomy reservoir
• Proper functioning of vent pump should be checked before connecting patient
to CPB.

24

25. MONITORING COMPONENTS
25
MONITORING DEVICE FUNCTION
Low- level alarm Alarms when level in the reservoir reaches
minimum running volume
Pressure monitors (line pressure, blood
cardioplegia pressure and vent pressure)
Alarms when line pressure exceeds set limits
Bubble detector (arterial line & blood
cardioplegia)
Alarms when bubbles are sensed
Oxygen sensor Alarms when oxygen supply to the oxygenator
fails
SaO2, Svo2 and Hb monitor Continuous measurement
In- line blood gas monitoring Continuous measurement of blood gases from the
ECC
Perfusionist Constantly monitors the CPB machine & ECC

26. SEQUENCE OF EVENTS DURING BYPASS
Circuit selection and priming
Anticoagulation
Cannulation
Initiation and maintenance
Myocardial Protection
Weaning and termination
26

27. CIRCUIT SELECTION AND PRIMING
• Highest flow that may be required for the procedure- 2.4- 3 L/min/m2 or 60-
70mL/kg/min
• Components of ECC- highest blood flow rate is desirable with acceptable hydraulic
forces enough not to cause trauma to the blood components
• Priming- de-airing of the CPB with mixture of crystalloids and colloids; causes
hemodilution- improves flow during hypothermia.
TCV = BVp +PV Target HCT- adult 21- 24%;
paediatric 28- 30%
• 20- 30% increase in patient’s intravascular volume on initiation of CPB; dilution of
proteins and formed elements but also alters the plasma level of drugs
HCTr = BVp x Hct
TCV
Blood required on prime = (HCTr x TCV) – (Pt. HCT x BVp)
HCT of donor blood
27

28. ANTICOAGULATION
• Heparinisation with 300- 400U/kg before arterial cannulation and initiation of CPB
• Advantages of heparin- rapid onset of action, rapid neutralisation by protamine, low
cost, safety
• Heparin resistance- >usual doses to achieve adequate anticoagulation; AT III
deficiency, HIT
• AT III deficiency- when >600U/kg heparin cannot achieve ACT >480s
• Baseline ACT (normal 80- 120s) must be noted; Target ACT 480s on-pump
• ACT (activated clotting time)- monitor anticoagulant effects of heparin
• Factors affecting ACT reading- hypothermia, hemodilution, coagulopathy,
thrombocytopenia, anticoagulants
• Heparin dosing may also be monitored using heparin dose response curves
• Alternatives- LMWH, Danaparoid, Lepirudin, Bivalirudin, Ancrod, Argatroban 28

29. INITIATION & MAINTENANCE
Check-
position of
ven
cannula &
patency of
art cannula
Ven clamps
released
CVP = 0,
arterial BP
50-90mm of
Hg, non
pulsatile
Art line
pressure of
ECC
<300mm of
Hg
Cerebral
oximetry
monitoring
Blood flow-
1.6-
3L/min/m2 ,
MAP- 50-
70mm of Hg,
SvO2 >70%
ABG x
30min,
correction if
Bdef<-5;
indicator to
increase
pump flow
and pressure
ACT x 30
min, heparin
bolus
administered
(at 24-30oC)
to maintain
400- 480s
Urine
output-
indicator of
adequacy of
perfusion
pressure and
flow
29

30. MYOCARDIAL PROTECTION
Aortic cross clamping
Bypass time >120min
Release of cross- clamp
Ischemia injury
Reperfusion injury
Ventricular fibrillation
LV distension
Excessive use of inotropes/ calcium
salts
Complete surgical repair with minimal
injury
Cardioplegia
Cardioplegic solution- energy substrates
Myocardial hypothermia (10-15oC)
Use of b-blockers, CCBs
LV decompression and de-airing
De-airing of coronary bypass graft
Judicious use of inotropes
DAMAGE
PROTECTION
30

31. WEANING & TERMINATION
• Patient rewarmed and de-aired
• Regular cardiac activity; if not pacemaker necessary
• Ventilation resumed, venous drainage slowed down,
volume returned back to heart from reservoir
• Once CO restored art pump flow reduced termination
• Once hemodynamic stability achieved protamine administration (Sentinel
event)
• 1- 1.3mg protamine for every 100U of heparin; slow administration to avoid
risk of hypotension
WEANING &
TERMINATION
SURGEON
ANAESTHESIOLOGIST
PERFUSIONIST
31

32. PHYSIOLOGICAL PARAMETERS OF CPB
Perfusion pressure during CPB
Pump flow during bypass
Temperature management
Acid- base management
Fluid management
32

33. PERFUSION PRESSURE DURING CPB
• Surrogate marker for organ perfusion, maintained between 50-70mm of Hg
• Cerebral perfusion pressure- MAP 50-150 mm of Hg; adverse neurological
outcomes- hypoperfusion (low) and embolism (high)
• During hypothermia, lower limit of cerebral autoregulation reduced to 20- 30
mm of Hg
• Severe atheromatous disease, systemic HTN , T2DM and elderly- higher
perfusion pressure for optimal perfusion
CPP
MAPTemperature
Alteration of pump flow
Volatile anaesthetics
Vasopressors
Vasodilators
ICP
Malposition of venous
cannula
Patient position
33

34. PUMP FLOW DURING BYPASS
Maintain O2 delivery at normal levels
for a given core temp
- Limit hypoperfusion
- Increases embolic load
Lowest flows enough not to cause end
organ injury
- Less embolic load
- Improved myocardial protection
- Better surgical visualization
• Pump flow and pressure depend on- hemodilution, temperature & arterial cross-
sectional area
• Pump flow at 1.2L/min/m2 – perfuse most microcirculation (with Hct- 22% and
hypothermic CPB); maintained between 1.6- 3.0L/min/m2
• Target mixed venous saturation >70%
34

35. TEMPERATURE DURING BYPASS
• Brain- most vulnerable to ischemic damage during CPB
• Deliberate hypothermia  Neuroprotection;
mechanisms-
1. Decrease in CMRO2
2. Attenuates release of glutamate and excitatory amino
acids
3. Reduces permeability of brain arterioles and prevents
BBB dysfunction
4. Suppression of inflammatory response
• Warm CPB (33-37oC) and cold CPB (23-32oC)
35
Sites of temperature
monitoring
Nasopharyngeal
Oesophageal
Tympanic membrane
Bladder
Rectum
Axilla
Sole of the foot
Pulmonary artery
Jugular bulb

36. WARM CPB COLD CPB
Advantages
1. Decreased bypass duration due to shorter rewarming
period
1. Protection against cerebral ischemia
2. Brain hyperthermia avoided during prolonged
rewarming
2. Decreased oxygen requirements
3. Near normal body temperature maintained 3. Allows lower flow rates
4. Early extubation 4. Decreased anaesthetic requirements
5. Less postop bleeding
6. Rapid recovery of normal cardiac rhythm
Disadvantages
1. Potential risk of cerebral damage 1. Impaired coagulation profile- increased bleeding
2. Increased requirement of vasopressors to maintain
MAP>50mm of Hg
2. Requires prolonged rewarming period
3. Large doses of vasopressors- renal vasoconstriction 3. Potential risk of brain hyperthermia
4. Impaired cerebral oxygenation if rewarming done
early. Uneven rewarming leads to ischemic injury
4. ‘After-drop’ due to incomplete rewarming
causing post-op shivers
6. Altered drug metabolism
36

37. • Aortic manipulation, cross-clamping and unclamping micro and macro
embolization to brain
• Hypothermia- initiated after onset of bypass; rewarming during weaning. Hence,
during these periods body temperature is similar in both warm and cold CPB.
• Rapid rewarming and hyperthermia cerebral injury
• Nasopharyngeal temperature not >37°C, acceptable range of 35.5°C–36.5°C
• Temperature gradient between the heater and venous blood not >10°C
• High gradient between core and peripheral temperature  ‘AFTER DROP’
• Vasodilators- homogenous rewarming
37
TEMPERATURE DURING BYPASS

38. BLOOD GAS MANAGEMENT
• temperature  solubility of CO2  Alkalosis ( by 1oC  pH by 0.015)
Alpha-stat strategy
• a refers to a-imidazole ring of histidine, an intracellular buffer
• constancy of charge on histidine regulation of all pH-dependent cellular
processes
• Temperature uncorrected
• Cerebral autoregulation, limits micro emboli; however, inhomogeneous cerebral
cooling 38




a-stat strategy
pH-stat strategy

39. BLOOD GAS MANAGEMENT
pH stat strategy
• constancy in pH and PaCO2 maintained despite temperature changes
• temperature corrected
• air-oxygen mixture “sweep speed” is reduced or carbon dioxide is added to the
oxygenator to increase PaCO2 and maintained at 40mm of Hg
• CO2 - potent cerebral vasodilator; homogenous cooling
• Uncoupling of cerebral autoregulation; cerebral blood flow despite metabolic
demand
• higher cerebral blood flow- chance of cerebral injury during rewarming,
embolization
39





40. FLUID MANAGEMENT
CRYSTALLOIDS
Adequate hemodilution allowing
cooling safely
Reduces colloid osmotic pressure
leading to extracellular water retention
COLLOIDS
Albumin coats circuit surfaces-
reducing interaction of blood
components, reduces platelet
activation and destruction
40

41. Initiator substances
Endotoxin, TNF, NF-
kB, anaphylotoxins,
cytokines
Effector cells
PMNs, platelets,
endothelial cells
Adhesion molecules
and release cytotoxic
oxygen radicals and
proteases
INFLAMMATORY RESPONSE TO CPB
• Physiologic insult of CPB  exaggerated, complex, pathologic immunologic events
• Passage of blood through ECC  activation of complement, platelets, neutrophils,
and pro-inflammatory kinins
41
Blood from ECC
reperfuses ischemic
organs
Local inflammatory
response in end organs
Whole-body inflammatory
response- complement,
fibrinolytic, kallikrein,
coagulation systems
ONSET END

42. END ORGAN EFFECTS
MYOCARDIUM
- O2 supply-demand mismatch
- Depletion of high energy
phosphate stores
- Intracellular calcium accumulation
- Ischemia- reperfusion injury
BRAIN
- Ischemic injury
- Micro and macro embolization
- Injury during rewarming
- Intracellular acidosis
RENAL
- Intravascular depletion and
hypoperfusion  renal ischemia
- Use of vasopressors
- Low pump flow rates  ischemia
GASTROINTESTINAL TRACT
- Splanchnic hypoperfusion
- Lack of autoregulation shunting
of blood away from GIT during
hypotension gut ischemia
- Increased mucosal permeability
- Impairs GI barrier function
ENDOCRINE
- Marked stress response
- Increased catecholamine levels
- Insulin, PG, renin release
- Vasopressin increases 20x
- Target glucose levels < 200mg/dL 42

43. 43

44. Care of Gravid patient during CPB
MATERNAL
• Monitoring uterine activity- Intraop,
postop and early ICU period
tocodynameter; intra-amniotic
catheter inadvisable in heparinized
patient;
• Intraop uterine contractions may be
deleterious to foetal O2 delivery;
preterm delivery
• Uterine contractions treated with
MgSO4, ritodrine
FOETAL
• FHR monitoring- ultrasonography,
phonocardiography, external
abdominal ECG
• Foetal ECG- foetal scalp electrode,
accurate but undesirable with
maternal anticoagulation
• POG>16wks, record FHR, FHR
variability and uterine contractions
• Onset of CPB- fall in FHR  during
CPB below normal termination –
foetal tachycardia
44

45. Strategies during cardiopulmonary bypass to improve foeto-
maternal outcomes
• Uterine tone monitoring
• FHR , if foetus >16 weeks gestation
• 15° left lateral tilt to prevent aortocaval compression >20 weeks gestation
• Maternal haematocrit >25%
• High maternal oxygen saturation
• Normothermia
• High perfusion flow rates (>2.5 L/min/m2)
• High perfusion pressure (>70 mm Hg)
• Minimize cardiopulmonary bypass time
• Pulsatile perfusion
• α-stat pH management
• Tocolytic therapy (magnesium sulphate, β2-agonists, progesterone supplementation
and intravenous alcohol infusions)
• Neonatologist and obstetrician on standby for emergency delivery 45

46. KEY POINTS
• Cardiopulmonary bypass (CPB) provides extracorporeal maintenance of respiration
and circulation at hypothermic and normothermic temperatures.
• CPB permits the surgeon to operate on a quiet, or non-beating, heart at hypothermic
temperatures, thus facilitating surgery in an ischemic environment.
• CPB is associated with a number of profound physiologic perturbations. The central
nervous system, kidneys, gut, and heart are especially vulnerable to ischemic events
associated with extracorporeal circulation.
• Perfusion should be adequate to support ongoing oxygen requirements; mean arterial
pressures of more than 70 mmHg may benefit patients with cerebral and/or diffuse
artherosclerosis. Arterial blood temperatures should never exceed 37.5°C.
• The initiation and termination of CPB are key phases of a cardiac surgery procedure,
but the anaesthesiologist must remain vigilant throughout the entire bypass.
46

47. SUMMARY
• Cardiopulmonary bypass machine has made complex cardiac
surgeries possible in modern day medicine.
• Understanding the anatomy of the heart-lung machine and its
physiological effects on the vital organs plays a crucial role in both
perioperative and postoperative period.
• It requires the anaesthesiologists, surgeons and perfusionists to
work as a team to conduct smooth initiation and termination of
cardiopulmonary bypass.
47

48. REFERENCES
• Ronal D. Miller, Miller’s Anaesthesia, 8th edition, Vol II, page: 2016- 2043
• Kaplan’s Cardiac Anaesthesia, 5th edition, page: 513- 544
• Morgan and Mikhail’s Clinical Anaesthesiology, 6th edition, page 443-474
• Cardiopulmonary Bypass: HISTORICAL DEVELOPMENT OF CARDIOPULMONARY BYPASS IN
MINNESOTA [Internet]. Tele.med.ru. 2019 [cited 20 November 2019]. Available from:
http://tele.med.ru/book/cardiac_anesthesia/text/gr/gr001.htm
• Sarkar M, Prabhu V. Basics of cardiopulmonary bypass. Indian J Anaesth 2017;61:760-7.
• Jameel S, Colah S, Klein A. Recent advances in cardiopulmonary bypass techniques. Continuing
Education in Anaesthesia Critical Care & Pain. 2010;10(1):20-23.
• O'Carroll-Kuehn B, Meeran H. Management of coagulation during cardiopulmonary bypass.
Continuing Education in Anaesthesia Critical Care & Pain. 2007;7(6):195-198.
• Machin D, Allsager C. Principles of cardiopulmonary bypass. Continuing Education in Anaesthesia
Critical Care & Pain. 2006;6(5):176-181.
• Shaaban Ali M, Harmer M, Kirkham F. Cardiopulmonary bypass temperature and brain function.
Anaesthesia. 2005;60(4):365-372.
• Kratz A, Van Cott E. Activated Clotting Time. Point of Care: The Journal of Near-Patient Testing &
Technology. 2005;4(2):90-94.
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