1. Perioperative Optimisation + oxygen delivery
Rob Stephens
PACU Study Day
Feb
PACU

2. Contents High risk surgery O2 O2 delivery + consumption
Postoperative physiology
Postoperative O2 delivery + consumption
‘Optimisation’
POM-O & Optimize

3. The High Risk Patient
Perioperative mortality is <1%, but increased to 33% in the high risk patient
High risk patients account for only 12.5% of surgical procedures, but also of >80% postoperative deaths
<15% of these patients were admitted to ICU
Scoring systems can help identify patients who are at high risk of postoperative morbidity and mortality
Patient Procedure
The national confidential enquiry into patient outcome and death has quoted
Identifying the high risk group would mean we could plan their management and reduce post op mortality

4. Patient factors; eg ASA Score
1 A normal healthy person
2 A patient with mild systemic disease
3 A patient with severe systemic disease that is not incapacitating
4 A patient with incapacitating disease that is a constant threat to life
5 A moribound patient who is not expected to live 24 hours with or without surgery
E An emergency operation
Hypertension, DM
COAD with moderate ex tolerance
COAD or severe angina with poor ex tolerance
Many scoring systems have been developed over the years that aim to quantify the risk of perioperative mortality.
ASA: subjective and also fails to take into consideration the surgery specific risk.
mortality

5. Combined scores; eg RCRI
High-risk surgery (i.e., intraperitoneal, intrathoracic, vascular)
Coronary artery disease
Congestive heart failure
History of cerebrovascular disease
Insulin treatment for diabetes mellitus
Preoperative serum creatinine level >180 μmoL
Very low 0 0.4
II. Low 1 0.9
III. Moderate 2 6.6
IV. High

6. Procedure Factors Body cavity entered eg laparotomy Blood loss
Length of procedure
Emergency/urgent vs elective/scheduled

7. Oxygen needed for cells to perform ‘work’ + live
only a few seconds of stored 02
surgery causes cells to need more 02 early- immediately postoperative phase
….Do patients that can give their cells more 02
?do better
C6H12O6 + 6O > energy + 6H2O + 6CO2
ATP

8. Oxygen Delivery DO2 = (HR x SV) x 1.34 x Hb x SaO2 DO2
The amount of oxygen delivered to the tissues per minute
DO2 =
1.34 x Hb x SaO2
100
DO2 = (HR x SV) x 1.34 x Hb x SaO2
Cardiac Output
Arterial Oxygen content CO
X CaO2
HR x SV
O2 must be transported effectively from the atmosphere to the tissues in order to sustain normal metabolism.
The amount of oxygen delivered to the tissues per minute irrespective of blood flow
Oxygen content of arterial blood (CaO2)
4 variables that can be manipulated to achieve the optimal DO2
Global DO2 depends on o2 sats rather then partial pressure: this is because of the sigmoid shape of the oxygen dissociation curve. There’s not much point having a PaO2 >9, as >90% of the haemoglobin is saturated with o2.
Although it may seem appropriate to transfuse patients to polycythaemic levels as a way to increase DO2, blood viscosity markedly increases above 10. this impairs blood flow and o2 delivery, particularly in the smaller vessels, exacerbating tissue hypoxia. therefore we aim for Hb 7-9, and the traditional 10 in patients with CAD.
Once patients have been transfused to the desired Hb, and oxygen supplementation has been given, its actually the co that is most often manipulated to achieve the desired DO2.

9. Oxygen Consumption
VO2
Total amount of oxygen consumed /taken up by the tissues per minute
VO2 = CO x (CaO2 – CvO2)
OER = VO2 CI = CO/body surface
(Oxygen extraction ratio) DO2 area
Cardiac Output
Arterial Oxygen content
Mixed Venous Oxygen content
~ 250ml/min in a normal adult undertaking routine activites.
It can be measured directly from inspired and expired o2 concentrations and expired minute volume or it can be derived from the CO.
The amount of oxygen consumed as a fraction of the oxygen delivery

10. Oxygen Consumption VO2 Can measure in breath:
Total amount of oxygen consumed or taken up by the tissues per minute
Can measure in breath:
O2 in – O2 out
Exercise mimics perioperative ‘stress’
As body tries to increase DO2
~ 250ml/min in a normal adult undertaking routine activites.
It can be measured directly from inspired and expired o2 concentrations and expired minute volume or it can be derived from the CO.
The amount of oxygen consumed as a fraction of the oxygen delivery

11. CPEx Exercise test: VO2

12. Oxygen Delivery: observation
Shoemaker et al : high risk patients who survived surgery exhibited certain higher haemodynamic variables:
CI > 4.5l/min/m2
DO2I > 600ml/min/m2
VO2I > 170ml/min/m2
Mechanism ?:
surgery causes cellular hypoxia
Patients who can ↑ oxygen delivery;  cellular hypoxia
↑survival
Having identified the high risk patients, there are still patients who survive and those that don’t survive. But what makes these two groups different?
The basis behind this was that during surgery, the human body is put under considerable stress and this can leave it hypoxic. Furthermore, critical illness the body cannot utilise oxygen effectively, leaving it more hypoxic.
By increasing the oxygen delivery, we are relieving this hypoxia and therefore increasing survival in high risk patients.

13. Prospective randomised, controlled trial
Oxygen Delivery: intervention
Prospective randomised, controlled trial
(Shoemaker et al, 1988)
CVP control PAC control PAC protocol
CI > 4.5l/min/m2
DO2 I > 600ml/min/m2
VO2I > 170ml/min/m2
23% % 4%
mortality mortality mortality
the results showed that using the supranormal levels as therapeutic goals significantly reduced mortality, reduced complications, reduced ICU and hospital stay
Thus the concept of goal directed therapy was born.

14. Prospective randomised, controlled trial
Oxygen Delivery: intervention
Prospective randomised, controlled trial
(Pearse et al, 2005)
LIDCO control LIDCO protocol
68% %
Complications Complications
Stay 14 days stay 11 days
the results showed that using the supranormal levels as therapeutic goals significantly reduced mortality, reduced complications, reduced ICU and hospital stay
Thus the concept of goal directed therapy was born.

15. Goal Directed Therapy (GDT)
Using therapeutic goals to guide management of oxygen delivery in high risk patients
Shoemaker et al, conducted the 1st outcome trial of GDT
Other studies confirmed that GDT improved survival in high risk patients (eg Singer + Mythen)
GDT has limitations
Only beneficial in early ‘shock’ /postop/ intraoperative
Not beneficial and possibly harmful in ‘late’ shock
Gattinoni : large randomised controlled study
When the patient could mount an increased CO in response to fluids and ionotropes
But when late shock was established, mycoacrdium is at it most vulnerable and there is increased endothelial permeability.
And aggressive fluid loading leads to widespread tissue oedema impairing pul gas exchange and tissue oxygen diffusion.

16. Oxygen Delivery
DO2
The amount of oxygen delivered to the tissues per minute
DO2 =
1.34 x Hb
100 CO
X CaO2 HR
x SV
x SaO2
O2 must be transported effectively from the atmosphere to the tissues in order to sustain normal metabolism.
The amount of oxygen delivered to the tissues per minute irrespective of blood flow
Oxygen content of arterial blood (CaO2)
4 variables that can be manipulated to achieve the optimal DO2
Global DO2 depends on o2 sats rather then partial pressure: this is because of the sigmoid shape of the oxygen dissociation curve. There’s not much point having a PaO2 >9, as >90% of the haemoglobin is saturated with o2.
Although it may seem appropriate to transfuse patients to polycythaemic levels as a way to increase DO2, blood viscosity markedly increases above 10. this impairs blood flow and o2 delivery, particularly in the smaller vessels, exacerbating tissue hypoxia. therefore we aim for Hb 7-9, and the traditional 10 in patients with CAD.
Once patients have been transfused to the desired Hb, and oxygen supplementation has been given, its actually the co that is most often manipulated to achieve the desired DO2.
Fluid
Inotropes
Be careful!
Controversial
? Transfuse
Fi02 ?Adequate ventilation

17. Role of Inotropes in GDT
Some patients achieve their target ‘goals’ with fluids alone
Wilson et al showed that mortality was reduced (3% vs. 17%) when dopexamine or adrenaline are titrated to achieve target goals
Dopexamine reduces complications and hospital stay compared to epinephrine
Inotropes can be harmful
Ionotropes can alter regional blood flow, tissue hypoxia and even myocardial ischaemia
Dopexamine: reduces gut hypoperfusion

18. PACU + GDT Although GDT: small studies successful
Does it work in the real world?
2 Studies coming to you……
Post Operative Morbidity Oxygen Optimisation POM-O
OptimiZe

19. OptimiZe Rupert Pearce RLH + Kathy Rowan ‘ICNARC’ Multi centre
Different surgery types/ anaesthetists / ICU’s etc
Run from ‘ICNARC’
Intensive Care National Audit & Research Centre
600 patients

20. OptimiZe Single blinded RCT – 2 groups standard & intervention
Commonly agreed goals eg
SaO2 94%, Hb>8−10 g/dl, temperature 37 °C, heart rate <100
Anaesthetists choice: extra fluid, vasoactive drugs, epidural/PCA
‘Intervention’ Above +
LiDCO-arterial waveform analysis: Arterial
250ml colloid challenge vs Stroke Volume
0.5 mcg/kg/min 30 minutes after fluid CVP

21. OptimiZe 50 years + and over
major gastrointestinal tract surgery > 90 mins
And 1+ of
Urgent / emergency surgery
Renal impairment (serum creatinine 130 μmol/l)
Risk factors for CVS/RS disease (see protocol)
Exclusion criteria ..includes
Acute MI/ Pulmonary Oedema/ Septic shock
Decline consent, pregnant

22. OptimiZe
% patients developing post−operative complications within 28 days of surgery
Duration of hospital stay
Post−operative critical care free days
Day 8
Post−operative morbidity survey for in patients ‘POMS’
Day 28
Infectious complications
Mortality
Quality of life (EQ5D health status )
Day 180

23. Summary
High risk patients account for >80% of postoperative death
Scoring systems can be used to identify high risk patients
Goal directed therapy reduces mortality, but needs to be started early
Inotropes should be used when patients cannot achieve their target goals with fluids alone
Ensure adequate Sa02 and
?transfusion -Hb should be considered
Studies coming to you soon!

24. The Oxygen Consumption and Delivery Relationship in Health
200
100
Oxygen consumption (VO2) (ml/min)
Critical DO2 B C
DO2 supply independent
OER = VO2
DO2
DO2 supply dependent
VO2 = 250ml/min in a normal healthy person undergoing normal activities of daily living. This equates to a oer ~25%
If the DO2 should fall for any reason, we increase our oer to maintain the same VO2.
The way we increase our oer is by dilating the microvasculature in our bodies to supply more oxygen to cells
VO2 remains relatively stable over a wide range of DO2, so BC on the graph is termed the o2 supply independent part.
Eventually, maximum oer is reached, and cannot increase further. is thought to be ~70%
This is called the critical DO2.
Because further reduction in do2 at this point will result in an oxygen debt, and anaerobic respiration will need to kick in and we start producing lactic acid. A
400
800
1200
Oxygen delivery (DO2) (ml/min)
Adapted from Thorax 57 (2):170, Leech and Treacher

25. The Oxygen Consumption and Delivery Relationship in Critical Illness
200
100 F
Oxygen consumption (VO2) (ml/min)
Critical DO2 E B C
OER = VO2
DO2
In critical illness, an altered global relationship between o2 consumption and delivery is thought to exist. This is shown with the broken line on the graph.
In critical illness, cells have difficulty in extracting and using oxygen, so the slope of the max. oer falls, which can be seen by line DE.
The other differnce is that the graph does not plateau as in the normal relationship.
Instead vo2 continues to rise to supranormal levels of do2 , so that the oxygen debt will only be relieved by increasing the do2
It is these supranormal levels of do2 shoemaker identified as increasing survival in high risk patients. A D
400
800
1200
Oxygen delivery (DO2) (ml/min)
Adapted from Thorax 57 (2):170, Leech and Treacher

26. References
Goldman L, Caldera DL, Nussbaum SR, Southwick FS, Krogstad D, Murray B, et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977;297:845-50