Pressures monitored during CPB
Normal arterial blood pressures at various stages of CPB
Flows at different temperatures
Flow in relation to cerebral flow auto-regulation and “safe” pressures
that patients require
Calculation of adequate flow at varying temperature
Value of venous & arterial blood sampling in the determination of
adequate flow [during CPB]
Pharmacological agents used to manipulate BP (on CPB)
|
|
Pre CPB |
CPB |
Coming Off |
|
Pre Oxygenator |
|
approx
X2 CPB arterial-line dependent
on oxygenator |
|
|
CPB arterial-line |
If
opened to aorta, indicates aorta pressure |
Dependent
on aortic pressure, tube length, diameter, blood viscosity |
If
opened to aorta, indicates aorta pressure - useful due to underestimation of
radial pressure |
|
Radial artery |
Normally
exceeds aortic pressure 10% |
|
Due
to uneven & intense vasodilation in arms underestimates aortic pressure |
|
Pulmonary artery diastolic |
10-15
mmHg ventilated
patient |
0
mmHg Increased
with LV filling (bronchial blood flow, AR) |
10-15
mmHg ventilated
patient |
|
Left atrial |
approx
10 mmHg |
0
mmHg Increased
with LV filling (bronchial blood flow, AR) |
approx
10 mmHg |
|
Central venous |
<10
mmHg |
0
mmHg Increased
with obstruction to venous floe |
<10
mmHg |
|
Coronary sinus |
|
<
40 mmHg when running cardioplegia |
|
|
Cardioplegia |
|
Ostial:
< 300 mmHg Sinus
< 100 mmHg Aortic
root < 200 mmHg |
|
1.
Phase of initial total CPB:
warm, aorta not X-clamped
a)
Patient
with normal flow autoregulation
i)
Although
heart is beating, it is empty thereby improving coronary perfusion gradient and
reducing myocardial work
ii)
>
50 mmHg
b)
Patient
with altered flow autoregulation
i)
Arteries
unable to dilate to maintain flow to distal bed in heart, kidney, brain
ii)
>
70 mmHg
2.
Phase of hypothermic CPB:
aorta X-clamped
a)
Patient
with normal flow autoregulation
i)
Heart
is isolated from systemic flow; higher pressures (MAP > 70) increase non
coronary collateral flush out of cardioplegia
ii)
50
mmHg
b)
Patient
with altered flow autoregulation
i)
As
heart is isolated, concern is with adequately perfusing brain & kidneys
ii)
mmHg
iii)
Observe
urine output
3.
Phase of rewarming: aortic
side biter in place
a)
Expect
transient hypotension immediately after X-clamp removal due to washing out of
myocardial metabolites & perfusion of dilated coronaries
b)
?
Avoid early post X-clamp removal hypertension to reduce reperfusion injuries
c)
Patient
with only saphenous vein grafts
i)
No
new perfusion to diseased coronaries at this stage as proximal anastomosis not
yet open
ii)
Scenario
similar to Initial warm CPB
iii)
If
significant coronary stenosis not supplied by IMA &/or significant renal,
brain vessel dx:
a)
MAP
70 - 90 mmHg
d)
Patients
with IMA
i)
New
source of perfusion to heart
4.
Phase of warm CPB: aorta not
clamped, heart revascularised
a)
MAP
similar to those expected after CPB
b)
Again,
consideration of:
i)
Vessel
disease to organs
ii)
Patient’s
normal BP
|
|
Cardiac Indexes with hypothermia |
|
|
|
Temperature
(°C) |
Cardiac
index [l/min/m2] |
|
|
34—37 |
2.4 |
|
|
30—34 |
2.0 |
|
|
25—30 |
1.8 |
|
|
20—25 |
1.5 |
|
|
<18 |
1 |
1.
Effects
of hypothermia on biochemical reactions
a)
Q10
» 2
i)
For
each 10° drop in temperature, the rate of metabolic rate or O2
consumption is roughly halved
2.
Hypothermia
permits the use of lower blood flows
a)
Reduced
blood trauma
b)
Permitting
longer safe CPB
i)
Emergency
pump shut off
c)
Reduced
blood return to heart
i)
Reduced
non coronary collateral flow
ii)
Drier
operative field
d)
Cooler
heart
i)
Reduced
myocardial ischaemia
1.
Cerebral autoregulation
a)
Normal
patient 37°C:
i)
Cerebral
blood flow [CBF] remains constant at 50ml/100g/min over a wide range of MAP 50
to 150 mmHg
b)
Normal
patient < 37°C (or some anaesthetics):
i)
CBF
remains constant at an appropriately reduced flow (<50ml/100g/min) over a
wide range of MAP < 50 to < 150 mmHg due to reduced brain metabolic rate
ii)
See
a lower autoregulatory plateau
iii)
With
intact autoregulation, adequate blood flow can be delivered at a lower
perfusion pressure during conditions of reduced metabolic rate
2.
Loss of Cerebral
autoregulation
a)
Consequences:
i)
Pressure
passive CBF
ii)
Hypotension
increases risk for cerebral hypoperfusion
b)
Examples
i)
Diabetes
mellitis
ii)
Cerebrovascular
disease (most > 70 yr)
iii)
pH-stat
management
iv)
Profound
hypothermia
v)
Deep
hypothermic circulatory arrest
a)
And
for several hours after
c)
Autoregulation
& temperature
(alpha-stat + patient with
no cerebrovascular disease)
i)
Range
28—30°C
a)
CPP
range of 20—100 mmHg
ii)
Range
15—20°C
a)
Loss
of autoregulation
b)
Hypothermia
induced vasoparesis
iii)
Raised
CVP
a)
Dissociation
between MAP & CPP

Cerebral
autoregulation curves
1.
Physiological
significance
a)
Reflects
impedance of the systemic vascular tree
b)
Assumes
laminar flow of homogenous fluid
2.
Formula

3.
Normal
values
a)
700—1600
dynes×sec×cm-5
4.
Clinical
considerations
a)
With
impaired LV function or valvular regurgitation, SVR should be reduced to the
lowest level while maintaining adequate BP for organ perfusion
i)
Reducing
the aortic impedance improves the LV ejection and lowers systolic LV wall
stress and myocardial O2 demand.
ii)
Impedance
is related to BP & SVR; lowering SVR can result in increased CO with no
change in BP
|
|
Cardiac Indexes with hypothermia |
|
|
|
Temperature
(°C) |
Cardiac
index [l/min/m2] |
|
|
34—37 |
2.4 |
|
|
30—34 |
2.0 |
|
|
25—30 |
1.8 |
|
|
20—25 |
1.5 |
|
|
<18 |
1 |
Lower limits
for pump flow
Awake patient: > 2.4 l/min/m2
Normothermic CPB: > 2.2 l/min/m2
With increasing hypothermia,
O2 demands decrease, pump flows may be reduced significantly

·
Exceeding
2.2 l/min/m2 pump flow at normothermia will not result in increased
tissue O2 consumption and increases the blood to greater damage from
higher shear rates
·
Reducing
the pump flow to below 2.2l/min/m2 at normothermia will limit the
amount of oxygen delivered to the tissues resulting in ischaemia
1.
Monitoring
adequacy of tissue perfusion during CPB
a)
Best
indicator is absence of significant postoperative organ dysfunction
i)
But
how to assess intraoperatively?
b)
Measurement
of actual tissue PO2
i)
Difficult
to ascertain in a clinical setting
ii)
Therefore
use less precise measures of perfusion adequacy:
2.
Global
measures of perfusion adequacy
a)
Not
on CPB
i)
CaO2
& O2 consumption are constant and independent of perfusion
ii)
Therefore,
CvO2 varies directly with changes in cardiac output
a)
Is
a useful index of perfusion as:
(1)
VO2
= Q (Ca O2 — CvO2)
(2)
![]()
(3)
VO2:
[O2 consumption]
(4)
[cardiac
output]
(5)
CaO2:
[O2 content of arterial blood]
(6)
CvO2:
[O2 content of venous blood]
b)
On
CPB
i)
CvO2
varies with varying temperature
ii)
Cardiac
output (Q) is under control of perfusionist
iii)
Microcirculation
function may not be normal
a)
Shunting
of blood past closed vascular beds results in increased CvO2 despite
reduced tissue perfusion
iv)
High
CvO2 may indicate:
a)
Excess
cardiac output
b)
Hypoperfusion
with shunting past closed microvasculature
v)
VO2
considers both cardiac output & O2 consumption is a better index
of perfusion
a)
Normal
VO2 at any temperature usually indicate at least adequate tissue
perfusion
b)
But
what is the normal VO2 for a particular patient & temperature?
c)
Total
systemic VO2 is a function of:
(1)
age
(2)
size
(BSA or lean body mass)
(3)
temperature
d)
Adult:
4ml/kg/min
e)
Infant
8ml/kg/min