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Created on - 29 May, 2016




  • Priming of CPB circuit is done to maintain fluid continuity between the patient and the CPB machine. Air column or air bubbles are totally removed by priming.
  • In adults,priming volume is 1.5 to 2 litres
  • Prime may be crystalloid or crystalloid combined with blood or colloid.
  • Disadvantage of priming is it causes hemodilution.
  • Patient’s PCV is reduced to approximately 25% with increase in plasma volume of 40% to 50%.
  • The degree of hemodilutional anemia that is observed on bypass is related to the patients’ initial red cell mass (body size and hematocrit) and priming volume of the ECC.

Hemodilution:- occurs as a result of priming of CPB circuit which leads to-

  1. Decrease protein binding as decrease in albumin and alpha 1 glycoprotein which has implications for protein binding of drugs due to alterations in bound to free drug ratio.
  2. Decrease RBCs – for drugs that are sequestrated in RBCs
  3. Decrease in amount of free drug
  4. Alteration in organ blood flow

History -

Done with blood initially- sanguineous prime

Gibbon,Kirklin with whole blood and high flows

Lillehei whole blood and low flow

Dewall with 5% D using hemodilution and hypothermia

Greer with 5% using hemodilution and hypothermia

Cooley with 5% using hemodilution and hypothermia

Panico/Nephine with saline solution using hemodilution and hypothermia

Long with Dextran & 5% albumin using hemodilution and hypothermia


Advantages of Hemodilution -

  1. Decrease blood viscosity
  2. Improved microcirculatory blood flow
  3. Increase regional blood flow
  4. Increase oxygen delivery to tissues
  5. Decrease blood products usage
  6. Increase blood flow at lower perfusion pressures ( lower shear stress)
  7. Reduced risk of hypertension during higher pump flows
  8. Beneficial in Jehovah’s witness patients

Physiological Consequences -


1)Rheology of blood –

Shear stress : Force applied to the liquid between 2 plates sufficient enough to set the liquid in motion is called shear stress.

Shear rate : Velocity with which the liquid moves between 2 plates is called is called velocity gradient or shear rate.

Shear stress = viscosity. shear rate

For most uniform fluids like water, viscosity is constant are called Newtonian fluids.

Viscosity of blood is not constant, depends on shear rate while flowing called as Non- Newtonian fluid.

High viscosity is associated with lower shear rates because the cellular elements and plasma proteins tend to aggregate, form rouleaux and decrease flow.

Other concept of behaviour of fluids –

The amount of shear stress that must be applied to the stationary Newtonian fluid to begin its movement is zero.

For Non- Newtonian blood- because of cellular geometry and aggregation, a force is required to start flow.It is called as ‘yield stress’.

At low shear rates- yield stress represents the viscous resistance and it depends on fibrinogen and haematocrit.


2)Circulatory effects -

Flow (Cardiac output) = Perfusion Pressure/ Total Peripheral Resistance

Flow (Cardiac output) = Perfusion Pressure/ Vascular Resistance . Viscosity

The Vascular Resistance is from smaller vessels- arterioles,venules,capillaries.

As vessel diameter decreases shear rate decreases and because viscosity is inversely related to shear rate, viscosity increases as flow decreases.As a result peripheral resistance also increases. Flow is lowest and viscosity highest in post capillary venules.

This physiologic effects are harmful if CPB is conducted without considering viscosity.

On CPB, decrease in flow rate and decrease in perfusion pressure , would increase viscosity and peripheral resistance,this will decrease perfusion.

Hemodilution- limits this adverse effect by decreasing viscosity

Because there is direct relation between viscosity and haematocrit, decreasing haematocrit decreases total resistance and increases perfusion.

Hemodilution is associated with decreased viscosity and decrease systemic vascular resistance and promotes microvascular blood flow.

Hypothermia – also influences the rheologic behaviour of blood.It decreases flow by inducing direct vasoconstriction and increasing viscosity.

Temperature decrease of 10 degrees - 20-25% increase in viscosity.


3)Hemodilution during CPB -

leads to uncoupling of normal relation between perfusion pressure and blood flow.


4)Hemodilution and drugs -

Hemodilution alters pharmacokinetics and pharmacodynamics of drugs by dilution and decreased protein binding.


5)Hemodilution and Oxygen transport -

Oxygen transport is expressed as a product of cardiac output and oxygen carrying capacity and is plotted against haematocrit.

Maximal oxygen delivery occurs at haematocrit of 30%

Delivery decreases approximately 10% below normal between 20 to 50%

Preservation of oxygen delivery is done by compensatory  increase in cardiac output.


6)Haemodilution and environmental effects -

Oxygen carrying capacity influenced by pH, pCO2, temperature,2 3DPG.

Metabolic acidosis, hypercarbia, hyperthermia, increased 2 3 DPG,anaemia cause shift to right.


7)Complications and hemodilution -

Neurological,Pulmonary complications like post perfusion lung, Renal failure - Hemodilution decreases morbidity of each of these organs.

Homologous blood syndrome : Blood diathesis causing multiorgan dysfunction, may be due to incompatibility and cross reactions between patient and multiple units used in prime.This is reduced with crystalloid priming and hemodilution.


8)Degree of Hemodilution -

Predicted on patients weight and haematocrit.

Blood volume can be calculated by –

multiplying patients weight by 7% in females and weight in kgs by 7.5% in males

Predicted Hct during CPB = Patient’s RBC volume before CPB (haematocrit in laboratory report)/ patients estimated blood volume (by above formula)+ preCPB IV fluid volume


9)Allowable Hemodilution -

Haematocrit < 30% preferred as > 30% is associated with decrease in microcirculatory flow

Normal prime volume- 1400-2100 ml

Factors affecting haematocrit on CPB –

  • Weight
  • Sex
  • Preoperative anaemia / polycythemia
  • Preoperative hypovolumia/ hypervolumia
  • CPB circuit volume
  • CPB prime volume
  • Pre CPB blood loss
  • Pre CPB volume distribution
  • Cardioplegia volume
  • Added prime to maintain flow

Allowable haematocrit in on pump CABG –

Important as < 15% haematocrit is associated with maldistribution of coronary blood flow away from the subendocardium.

>34% higher haematocrit led to risk of Q wave myocardial infarction,decreased LV function and increased mortality.

HCT <22% is associated with increases in risk of stroke, MI, low CO, cardiac arrest, renal failure, prolonged ventilation, reoperation for bleeding, sepsis, multi-organ failure, prolong ICU stay.


10)Hemodilution and Kidneys -

Acute renal failure or a significant increase in postoperative serum creatinine increases as hematocrit values decreases below 21%–24% on CPB.

HCT <24% on CPB is the “critical threshold” triggering significantly worsened renal outcomes.


11)Hemodilution and CNS -

cerebral blood flow increase in response to anemia  maintains adequate oxygen delivery.

HCT <19% during CPB is associated with >2x risk mortality

Increased cognitive decline in elderly patients managed on CPB with HCT 15-18% compared to HCT>27%.


12)Assessing adequacy of perfusion with Hemodilution -

Organ perfusion is monitored for adequacy

Cerebral function- EEG : global cerebral function

                             TCD : blood flow velocity

                              NIRS : oxygen saturation rSo2

Renal function- UO

ABG - oxygenator function

MVO2 - marker of adequate perfusion


References -

Cardiopulmonary bypass-Principles and Practice by Glenn P. Gravlee.

Kaplan’s Cardiac Anesthesia: The Echo Era 6th Edition

Hemodilution and Hematocrit on Cardiopulmonary Bypass: How Low Can We Go? Daryl Oakes.Society of cardiovascular anesthesia:

Optimal Perfusion During Cardiopulmonary Bypass: An Evidence-Based Approach. Glenn S, Murphy.International Anesthesia Research Society, vol 108:5,May 2009

Hemodilution and Hematocrit: How Low Do You Go?Joseph P. Mathew. SCA 31st Annual Meeting & Workshops April 18 – 22, 2009 


- by Dr Amarja

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