permissive hypoxemia by dr vishram buche

2. ………………!!!
Dr Vishram Buche
Dept Of Pediatric Intensive Care
Central India’s Child Hospital And Research Institute
Nagpur

3. Lung protective
strategy
Oxy/Baro.
trauma

4. PERMISSIVE HYPOXEMIA….. (PH)
PEEP
Prone ventilation
Lung recruitment manoeuvres (LRM)
Pressure controlled inverse ratio ventilation (PC-IRV)
Low TV and permissive hypercapnia1
2
3
4
5
6
………..

5. 2
3
4
5
1 Definition & Facts…….
Goals…….
Pathophysiology……
Visibility of Permissive hypoxemia….
Monitoring Permissive hypoxemia..?
6 Take home massage / conclusion….

6. ………

7. A rapid ↓ in CaO2 developing < 6 hrs
Acute
hypoxemia
↓ CaO2 occurring in 6 hrs to 7 days
(e.g., pneumonia)
Subacute
hypoxemia
↓ CaO2 for 7–90 days
(e.g., prolonged ARDS, high altitude)
Sustained
hypoxemia
Prolonged ↓ of CaO2 for over 90 days
(e.g., COPD)
Chronic
hypoxemia
Cross-generational ↓ CaO2
(e.g., Tibetan highland residents)
Generational
hypoxemia
Crit Care Med 2013; 41:0–0
:

8. ……..
3
2
1
Wilson DF, Erecinska M: The oxygen dependence of cellular energy metabolism.
Adv Exp Med Biol 1986; 194:229–239

9. How much ↓SaO2 is tolerated in the critically ill
is difficult to determine and still remains unclear
Targeting normoxemia…….. in acute situations,
NOT achievable/ beneficial in critically ill
patients with subacute or sustained hypoxemia
VO2 is governed by metabolic activity rather
than oxygen supply, but this relationship can be
modified during the inadequate oxygen supply.
6
5
4
Wilson DF, Erecinska M: The oxygen dependence of cellular energy metabolism.
Adv Exp Med Biol 1986; 194:229–239
……..

10. Prolonged hypoxia….VO2 ↓es 40 to 60%
(down-regulation of "non-essential" cellular processes)
↓ in VO2 not only attenuates the deficient DO2, but also
make cells less susceptible to hypoxic injury even if DO2
falls to critical level
This phenomenon is reversible on re-exposure to
normoxia and is not associated with demonstrable long-
term cellular harm. This is "oxygen conformance"
9
8
7
Wilson DF, Erecinska M: The oxygen dependence of cellular energy metabolism.
Adv Exp Med Biol 1986; 194:229–239
……..

11. ……..
" "
Exposure to subacute and sustained
hypoxemia permits a coordinated process of
adaptation, referred to as acclimatization.
It is unlikely that critically ill patients mount such
effective cardiorespiratory countermeasures to
increase oxygen delivery as a result of their
underlying pathology.
1
2
1.Levett DZ, Radford EJ, Menassa DA, et al;
Acclimatization of skeletal muscle mitochondria to high-altitude hypoxia during an ascent of Everest. FASEB J 2012; 26: 1431–1441
2.Levy RJ, Deutschman CS: Deficient mitochondrial biogenesis in critical illness: Cause, effect, or epiphenomenon? Crit Care 2007; 11:158
3.Ruggieri AJ, Levy RJ, Deutschman CS: Mitochondrial dysfunction and resuscitation in sepsis. Crit Care Clin 2010; 26:567–575, x

12. 1.Levett DZ, Radford EJ, Menassa DA, et al;
Acclimatization of skeletal muscle mitochondria to high-altitude hypoxia during an ascent of Everest. FASEB J 2012; 26: 1431–1441
2.Levy RJ, Deutschman CS: Deficient mitochondrial biogenesis in critical illness: Cause, effect, or epiphenomenon? Crit Care 2007; 11:158
3.Ruggieri AJ, Levy RJ, Deutschman CS: Mitochondrial dysfunction and resuscitation in sepsis. Crit Care Clin 2010; 26:567–575, x
……..
" "
Skeletal muscle biopsies of healthy volunteers exposed to
sustained hypoxia at high altitude……
1 Deactivation of mitochondrial biogenesis
2 Down-regulation of mitochondrial uncoupling,
…………….resulting in improved efficiency of ATP production.
Comparable changes in mitochondrial biogenesis also occur
in critically ill patients and may reflect similar adaptive
responses.
3
4

14. …relatively low SaO2,
while maintaining adequate DO2 ….
...the detrimental effects of high ventilatory support
on pulmonary and other systems as well
….morbidity and mortality in selected hypoxemic
patients who have had sufficient time to adapt this
low PO2
…
…
…

17. ….........

18. DO2 x (SaO2-SvO2) =
Oxygen
Balance
Oxygen
Delivery
DO2
VO2/DO2 is normally 25%
Rising VO2/DO2 ratio is a sign of inadequate tissue
oxygenation
Oxygen
Consumption
VO2
DO2 x (SaO2-SvO2) = = CO x CaO2
O2 demand

19. PaO2
SaO2
OXY (Sat) 98%
HAEMOGLOBIN
2 % Dissolved
Oxygen
O.
D.
C.PAO2
A.C.I.
CaO2
Content of oxygen
Ml/100 of blood
Delivery Of Oxygen
DO2
Cardiac output
……………
VO2

20. O2 unloaded from Hb
during normal
metabolism
O2 reserves that can be
unloaded from Hb
to tissues with increased
demands
20
15
10
5
0
Vol %
CaO2

21. ……………
DO2 Oxygen delivery ml/min
VO2
Oxygen consumption
ml/min
Delivery
dependant
consumption
Delivery Independant consumption
Lactic acid
Oxygen extraction O2ER
200
200 400 600
100
VO2-DO2 relationship….
250
C-DO2
60%............O2ER……………………….25%
300

22. Oxygen delivery DO2
Oxygen
consumption
VO2
Delivery
dependant
consumption
Delivery Independant consumption
Lactic acid
Oxygen extraction O2ER
200 400 600
Critic DO2
200
100
250
……………
VO2-DO2 relationship….

23. ……………
20
15
10
5
0
Vol %
CaO2
75
65
HbSaturation(%)
100
80
60
40
20
0 20 60 80 100
PO2 (mmHg)
40

24. Oxygen Therapy in Critical Illness
D S Martin; M Patrick William Grocott, Crit Care Med. 2013;41(2):423432
1.Precise control of arterial oxygenation
2.Permissive hypoxemia

25. Individualised
therapeutic target of O2
 Age
 Clinical setting
 Underlying disease
 Chronicity
 Comorbidities
Arterial oxygenation
Hypoxia Hyperoxemia
………….
Where do we stand ?

26. Permissive hypoxemia
target zone
H ypoxia H yper oxemia
……..
acclimatization
Arterial oxygenation
Individualised
therapeutic target of O2
hypoxemia
It Can Be done…..!!

27. ……..!!!!

28. Why do I have to allow patient to low O2..?
 Prone positioning
 HFOV
 Inhaled NO
 ECMO
 High FiO2
 High Positive pressure

29. ………..
1) Improved oxygenation but unchanged outcome
2) Deterioration in oxygenation but unchanged outcome
3) Improved outcome despite unchanged oxygenation

30.  Aims for an SaO2 ….. “82% -- 88%”, PaO2…. 60 - 75
 Not to direct a specific SaO2 goal but, rather, a careful
balance between the target SaO2 and the ventilatory support
required to achieve a higher SaO2
 The actual goal SaO2 will probably differ between patients
and vary in an individual patient over time

32. …………?

33. Cellular
O2 markers
Clinical 1
2
3
Abnormal skin perfusion,
↓ed urine output,
Hypotension.
Lactate……… Lacti-time?, pH
Mixed venous oxygen saturation (SvO2) < 50%
Mixed veno-arterial CO2 gradient
….VO2 < 180 ml/min or < 2.4 ml/kg/min
….(SaO2- SvO2) > 50%, O2ER < 60%
………………..

34. Gastric Intra mucosal pH
Real-time in vivo speckle laser
Near infrared spectroscopy (NIRS)
Fluorescence quenching
Micro dialysis

35. What are the potential risks
of permissive hypoxemia
Is permissive hypoxemia equally
tolerated by different organ systems

36. • The of optimum SaO2 goals is essential if cellular
hypoxia and hyperoxia as well (and ventilation) are to be
avoided.
• There are NO generally acceptable for the
lower limit of oxygenation that can be tolerated and individual
evaluation is crucial when determining prescribed targets.

37. and biomarkers ….. patient selection,
and provide an umbrella of safety with regards to tissue
oxygenation.
At present, any immediate change in clinical practice
toward permissive hypoxemia is in the
absence of experimental data in critically ill patients.
 Permissive Hypoxemia in critically ill patients should be
a high

38. The body can survive hypoxia by mean of " “
Permissive hypoxemia has a target end point
Bed side monitoring by pH, Lactate, SvO2 , O2ER…accepted
indictors for adequacy of tissue oxygenation

40. • Abdelsalam M. Permissive hypoxemia: Is it time to change our approach?
Chest 2006;129(1):210-211
• Guyton AC, Hall JE. Textbook of medical physiology: transport of oxygen and
carbon dioxide in the blood and tissue fluids.
Philadelphia: Mosby Elsevier Saunders; 2006:502-513.
• Mohamed Abdelsalam MD and Ira M Cheifetz MD FAARC
Goal directed therapy with ARDS : permissive hypoxemia
RESPIRATORY CARE • Nov 2010 Vol 55 NO. 11
• D S Martin : Oxygen therapy in critical illness :
Crit Care Med 2013;41(2): 423-432