Constituents of priming fluid
relative to patient size and priming volume of the oxygenator
Limitations and validity of
haemodilution
Formulae for calculation of
haemodilution
CO2 flushing prior to
priming the oxygenator
PreCPB filter placement and pore
size relative to priming
Inline monitoring of haemodilution
·
Due
to benefits of haemodilution and concerns about blood borne diseases, is
standard practice to use a nonblood CPB prime
·
Patients
< 35 kg may need some blood in prime to avoid excessive haemodilution
·
Haemodilution [Hct: 21-24%] reduces blood viscosity
resulting in:
·
increased
tissue perfusion
·
reduced
blood cell trauma
·
improved
renal function
·
reduced
need for homologous blood
1.
Osmolality
a)
Isosmotic
or slightly hypertonic to minimise tissue oedema
b)
Use
of mannitol or albumin
2.
Electrolytes
a)
Normal
electrolyte balance must be maintained to prevent post CPB electrolyte
abnormalities
3.
Volume
a)
Enough
volume to fill & prime:
i)
Circuitry,
oxygenator, filters, venous reservoir
b)
Enough
volume to enable safe conduct of perfusion:
i)
venous
level, flow rates required
c)
Not
too much volume to cause excessive haemodilution
4.
Haemodilution
a)
Avoid
< 18 % Hct
b)
To
determine the initial Hct on CPB:
![]()
Hctint
= initial Hct on CPB
EBV
= estimated patient blood volume
Hct
= preoperative Hct
c)
To
determine the volume of red blood cells needed to prime the circuit:
![]()
PBV = patient’s blood volume
ECCV = extracorporeal
circuit volume
CPBHct = desired Hct on CPB
PtHct = patient’s pre CPB
Hct
|
Estimate of total blood volume by age |
|
|
Age |
cc/kg |
|
Adult |
65 |
|
3 years |
70 |
|
1 year |
75 |
|
6 months |
80 |
|
Acceptable values for prime |
|
|
pH |
7.35-7.45 |
|
pO2 |
80-300 mmHg |
|
pCO2 |
35-45 mmHg |
|
Na+ |
< 140 mEq |
|
K+ |
3.5-5 mEq |
|
Ca2+ (ionised) |
approx 1 mmol |
|
Glucose |
< 200 mg/dl |
|
Hct |
Depends
on anticipated degree of hypothermia |
|
Oncotic press |
13-16 mmHg |
|
Osmotic press |
300 mOsm |
Avoid SPPS in vacuum primed
oxygenators (SciMed)
1.
Benefits of haemodilution
a)
Lowers
blood viscosity
i)
Counteracting
sludging effect of hypothermic blood
ii)
Improves
tissue perfusion during hypothermia
b)
Reduced
risks associated with blood transfusions
c)
See
appropriate modules
2.
Risks of haemodilution
a)
Reduced
MAP upon commencement of CPB
i)
Due
to reduced viscosity
b)
Lowered
colloid osmotic pressure
i)
Dilution
of plasma proteins
ii)
Require
increased I.V. fluid due to 3rd space shifts
c)
SaO2
must be kept at 100%
i)
To
prevent any decline in O2 transport
ii)
O2
transport = O2 content ´ blood flow
iii)
[O2
content = 1.34 ´ Hb ´ SaO2 + dissolved O2]
d)
Excessive
haemodilution
i)
Blood
flow cannot increase to compensate for reduced O2 content
ii)
Ischaemia
of critical organs
iii)
anaerobic
metabolism
e)
Increased
flow
i)
At
similar VO2 (O2 consumption rates), a halving of the Hct
requires a doubling of flow
ii)
Importance
of hypothermia to reduce VO2
iii)
If
normothermic, SvO2 may fall on CPB
f)
Factors
reducing ability of body to tolerate significant reductions in Hct:
i)
Stenosis
a)
Limits
maximum flow of blood
b)
Reduced
viscosity does help however
ii)
Cardiac
failure after CPB
a)
Unable
to maintain sufficient C.O. necessary to maintain adequate O2
delivery
iii)
Left
shifted O2-Hb curve
a)
Reduces
O2 release in tissues
b)
Hypothermia,
alkalosis, reduced 2,3 DPG
iv)
Lung
disease
a)
Unable
to maintain sufficient gas exchange necessary to maintain adequate O2
delivery after CPB
g)
‘Healthy’
patient
i)
Able
to tolerate down to Hct of 20

Hctint
= initial Hct on CPB
EBV
= estimated patient blood volume
Hct
= preoperative Hct
Blood
volume = Patient weight ´ 8% [infants]
7.5% [child,
adult male]
7.0 % [adult
female]
Red
cell volume = Blood volume ´ Hct
·
CO2
purging of the assembled circuitry prior to priming
·
Used
to displace atmospheric N2 which is difficult to debubble
·
Occurs
for several minutes
·
CO2
is used as has a high water solubility; any CO2 bubbles not washed
from the circuit during priming are quickly adsorbed
·
Recirculation
of the prime with a O2 gas flow allows for excessive CO2
to be removed from the circuit before commencing CPB
·
The
slightly unoccluded pump head will allow the CO2 to permeate the
pump boot
·
0.2
microns
·
Upstream
of arterial line
·
Removes
tubular and oxygenator dust and other debris, microbes and spores, early onset
spallation (silastic), particulate matter of what ever source
·
Positioned
where all the pump prime will flow, yet is removable prior to commencement of
CPB
Method
1
Method
2
|
Fluid |
grms/l |
(ml) |
Glu (g) |
kJ |
Na |
K |
Cl |
Ca |
Lactate |
pH |
Osmolality |
|
0.9% NS |
9 |
1000 |
— |
— |
154 |
— |
154 |
— |
— |
|
|
|
5% Dextrose |
5 |
1000 |
50 |
850 |
— |
— |
— |
— |
— |
4 |
278 |
|
Hartman’s |
|
1000 |
— |
— |
131 |
5 |
112 |
2 |
29 |
5 -7 |
278 |
|
Ringers |
|
1000 |
— |
— |
147 |
4 |
156 |
2.2 |
— |
|
309? |
• Readily available &
cheap
• Slightly hypotonic and
becomes steadily more so as the dextrose is metabolised leaving the patient
with a sizeable water load to excrete
• The marked dilutional effect
on plasma bicarbonate produces a marked systemic metabolic acidosis with
hyponatraemia & hypochloraemia
• Not recommended for
diabetics as may lead to very high glucose levels during CPB
• Due to its effect in raising
osmotic pressure in prime, may be associated with reduced postoperative fluid
retention & perioperative fluid requirements
• However, CNS damage may
occur with hyperglycaemia when associated with global or focal injury is
followed by immediate reperfusion of the ischaemic region [therefore should
avoid hyperglycaemia particularly in thoracic aortic repairs when are
subjecting global CNS ischaemia]
• Similar ion concentration to
plasma
• Lactate renders Hartman’s
slightly acid until liver converts lactate into bicarbonate, eventually
producing a metabolic alkalosis
• Diabetic patients are less
able to handle the lactate peripherally so that it is more readily converted to
glucose thereby exacerbating hyperglycaemia [use of NS or Ringer’s]
• Due to exchange of Na for K
in kidneys, may exacerbate hypokalaemia
• Danger of exacerbating any
metabolic acidosis by producing lactic acidosis, particularly in seriously ill
patients with poor tissue perfusion or impaired hepatic function
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