Hatem O.Qutub MD,FCCP,FCCM
 Definition
& Facts
 Goals
 Pathophysiology
 Visibility
of Permissive hypoxemia
 How to monitor Permissive hypoxemia
 Tack home massage / conclusion
 Permissive
hypoxemia is lung-protective
strategy, where by a relatively low
arterial oxygen saturation [SaO2] is
accepted .
 Hypoxemia
is not uncommon in critically ill
patients
 How low, how long and how fast would
hypoxia effect the outcome [ low SaO2 is an
independent predictor of mortality, however,
this relationship is more complicated in
established critical illness with sustained
hypoxemia. ]
 Severe hypoxemia can result in cellular
hypoxia, organ dysfunction, and death
 The
degree to which low SaO2reduction
can be tolerated in the critically ill is
difficult to determine and remains
unclear
 Targeting normoxemia may be the best
practice in acute situations, it may be
neither achievable nor beneficial in
critically ill patients exposed to subacute
or sustained hypoxemia
Cellular oxygen consumption (VO2) is governed
by metabolic activity rather than oxygen supply,
but this relationship can be modified during
conditions of limited oxygen availability.
 Following exposure to moderately prolonged
hypoxia, cultured cells demonstrate a 40 to 60%
reduction in VO2 secondary to the downregulation of "non-essential" cellular processes.
 This phenomenon is reversible on re-exposure to
normoxia and is not associated with
demonstrable long-term cellular harm. "oxygen
conformance,"

 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.
 In
skeletal muscle biopsies of healthy
volunteers exposed to sustained hypoxia at
high altitude, there is deactivation of
mitochondrial biogenesis and downregulation of mitochondrial uncoupling,
possibly resulting in improved efficiency of
ATP production.
 Comparable changes in mitochondrial
biogenesis also occur in critical ill patients
and may reflect similar adaptive responses.
Goal of Permissive Hypoxemia
 Minimize
the detrimental pulmonary and
systemic effects of high ventilatory
support
 Accepting a relatively low arterial
[SaO2]),while maintaining adequate DO2
 Reduce morbidity and mortality in
selected hypoxemic patients who have
had sufficient time to adapt this low PO2
stat
Oxygen
Delivery
Oxygen
Balance
Oxygen
Consumption
 Tissue
oxygenation → DO2 = V˙O2
 Hypoxia occur :
a- ↓ C.O (ischemic hypoxia)
b- ↓ Hb concentration(anemic hypoxia)
c- ↓ oxygen saturation (hypoxic hypoxia)
d- ↑metabolic demands of the body
• Cardiac
output (blood
flow)
• O2 content of
arterial
blood:
 Hemoglobin
 Oxyhemoglobin
saturation
 PaO2
Oxygen unloaded from
hemoglobin during normal
metabolism
Oxygen reserves that can be
unloaded from hemoglobin to
tissues with increased
demands
•Age
•Clinical setting
•Underlying
disease
•Chronicity
• Comorbidities
Because :
Therapy intervention upon facing low o2
[including high frequency oscillatory ventilation,
prone positioning, inhaled nitric oxide, and
extracorporeal membrane oxygenation
 Mechanical ventilation strategy's
Non have shown any :
1) improved oxygenation but unchanged outcome
2) improved outcome but unchanged oxygenation
3) deterioration in oxygenation but unchanged
outcome.


 Aims
for an SaO2 : “82% -- 88%”
 Not to direct a specific SaO2 goal but,
rather, a careful balance between the
target SaO2 and the ventilatory toxicity
required to achieve a higher SaO2
 The actual goal SaO2 will probably differ
between patients and vary in an
individual patient over time
 While
searching for the cause and its
complications :
1- Allow permissive hpercapenia
2- Avoid high platue pressure
3-Deal with refractory hypoxemia
4- Dealing with MV complications
5-Maintained acceptable hemodynamic
6- Minimized morbidity & avoid mortality
No data to support the assumption that improved
oxygenation will improved clinical outcomes in
patients with ARDS.
 Supplemental oxygen is a supportive
intervention serving to correct a consequence of
the underlying pathophysiology, rather than to
treat a cause or reverse a disease process.
 Cellular hypoxia is not a prominent feature of
ARDS.
 Death in ARDS patient is rarely due to
intractable hypoxemia or respiratory failure, but
commonly from the underlying cause of ARDS
(e.g., systemic inflammation due to sepsis)

How to monitor Permissive hypoxemia?
a-Indicate the adequacy of oxygen
transport
b-Represents the amount of oxygen
remaining in the systemic venous blood
after passing through the tissues
c-Reflects the balance between DO2 &
V˙O2
d-Surrogate for cardiac output
O2
ScvO2
SvO2
O2 Content
Venous
Arterial
Cardiac
Output
O2 Return
O2 Consumption
O2 Delivery
Capillary Beds
®
 Variables'
used to confirm adequate O2
for normalizing of :
 SvO2
 blood lactate
 base deficit
 Arterial pH
 Near
infrared spectroscopy
 Real-time in vivo speckle laser
 Microdialysis
 Fluorescence quenching





The selection of optimum arterial oxygenation goals is
essential if cellular hypoxia and unnecessarily excessive
oxygenation (and ventilation) are to be avoided.
There are no generally acceptable thresholds for the lower
limit of oxygenation that can be tolerated and individual
evaluation is crucial when determining prescribed targets.
The development of new technologies and biomarkers may
aid 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 not justified in the absence of
experimental data in critically ill patients.
Permissive Hypoxemia in critically ill patients should be a
high research priority .
The body can survive hypoxia by mean of
"acclimatization“
 Permissive hypoxemia has a target end point
 Bed side monitoring of [ PH,BD,L acid,Svo2] is
accepted indictors for adequate tissue
oxygenation
 "servo control" systems based on high quality
input variables, derived from a reliable pulse
oximetry source or continuous intra-arterial
oxygen tension monitoring, could be linked to
variable oxygen administration systems, to allow
real-time management of hypoxemia for
automated control of arterial oxygenation.
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Abdelsalam M. Permissive hypoxemia: Is it time to change
our approach? Chest 2006;129(1):210-211
Phillips BA, McConnell JW, Smith MD. The effects of
hypoxemia on cardiac output. A dose-response curve. Ches
1988;93(3): 471-475.
Grocott MP, Martin DS, Levett DZ, McMorrow R, Windsor J,
Montgomery HE. Arterial blood gases and oxygen content
in climbers on Mount Everest. N Engl J Med 2009;360(2):140149.
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
FAARCRESPIRATORY CARE • NOV 2010 VOL 55 NO 11
It is not impossible .
We can live with hypoxia.