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Hatem O.Qutub MD,FCCP,FCCM.  Definition & Facts  Goals  Pathophysiology  Visibility of Permissive hypoxemia  How to monitor Permissive hypoxemia.

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Presentation on theme: "Hatem O.Qutub MD,FCCP,FCCM.  Definition & Facts  Goals  Pathophysiology  Visibility of Permissive hypoxemia  How to monitor Permissive hypoxemia."— Presentation transcript:

1 Hatem O.Qutub MD,FCCP,FCCM

2  Definition & Facts  Goals  Pathophysiology  Visibility of Permissive hypoxemia  How to monitor Permissive hypoxemia  Tack home massage / conclusion

3  Permissive hypoxemia is lung-protective strategy, where by a relatively low arterial oxygen saturation [SaO2] is accepted.

4  Hypoxemia is not uncommon in critically ill patients  How low, how long and how fast would hypoxia effect the outcome [ low SaO 2 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

5  The degree to which low SaO 2 reduction 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

6  Cellular oxygen consumption (VO 2 ) 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 VO 2 secondary to the down- regulation 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,"


8  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.

9  In skeletal muscle biopsies of healthy volunteers exposed to sustained hypoxia at high altitude, there is deactivation of mitochondrial biogenesis and down- regulation 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.

10 Goal of Permissive Hypoxemia

11  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


13 Oxygen Balance Oxygen Balance Oxygen Delivery Oxygen Delivery Oxygen Consumption

14  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

15 Cardiac output (blood flow) O 2 content of arterial blood:  Hemoglobin  Oxyhemo- globin saturation  PaO 2

16 Oxygen unloaded from hemoglobin during normal metabolism Oxygen reserves that can be unloaded from hemoglobin to tissues with increased demands

17 Age Clinical setting Underlying disease Chronicity Comorbidities



20  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.

21  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


23  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

24  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)

25 How to monitor Permissive hypoxemia?

26 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

27 O2O2 SvO 2 O 2 Content O 2 Consumption ® ScvO 2 O 2 ReturnO 2 Delivery Capillary Beds VenousArterial Cardiac Output

28  Variables' used to confirm adequate O2 for normalizing of :  SvO2  blood lactate  base deficit  Arterial pH

29  Near infrared spectroscopy  Real-time in vivo speckle laser  Microdialysis  Fluorescence quenching

30  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.

31  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.

32  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):140- 149.  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

33 It is not impossible. We can live with hypoxia.

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