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OI = [mean airway pressure x FiO2 ÷ PaO2] x 100](https://image.slidesharecdn.com/oxygenationventilationdrsaneesh-180904061730/85/Oxygenation-ventilation-saneesh-15-320.jpg)
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Oxygenation ventilation # saneesh
This document discusses various concepts related to ventilation and oxygenation. It defines terms like hypoxemia, hypoxia, arterial oxygen saturation, and arterial oxygen tension. It describes how to evaluate for hypoxemia and discusses various causes of hypoxemia including hypoventilation, ventilation/perfusion mismatching, and right-to-left shunts. Various formulas related to oxygen delivery and measurements like the A-a gradient and oxygenation index are also outlined.
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Oxygenation ventilation # saneesh
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- 3. HYPOXEMIAHYPOXEMIA An abnormally lowlevel of oxygen in the blood (ie, low PaO2). HYPOXIAHYPOXIA Oxygen supply is inadequate • Whole body - general hypoxia • Local - tissue hypoxia
- 4. Arterial oxygen saturation(SaO2) Arterial oxygen tension (PaO2) A-a oxygen gradient PaO2/FiO2 ratio a-A oxygen ratio Oxygenation index
- 5.
- 6. Abnormal SaO2? Resting SaO2 ≤95% or exercise desaturation ≥5 percent O2supplementation target 94 -98%, COPD - 88 to 92%
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- 9. • • "A" = alveolaroxygenation "a" = arterial oxygenation
- 10. A-a oxygen gradient= PAO2 - PaO2 PAO2 is derived; PaO2 is obtained from ABG fraction of inspired oxygen (0.21 – room air) atmospheric pressure (760mmHg – sea level) partial pressure of water (47mmHg) arterial CO2 tension respiratory quotient 0.8
- 11. A-a gradient A-a gradient= 2.5 + 0.21 x age in years (Room Air) FiO2 Rise in PAO2 > PaO2 rise
- 12. High A-a gradient •Alveolar membrane diseases • Interstitial diseases • V/Q mismatch Normal A-a gradient Hypoxemia Hypoventilation with displacement of alveolar O2 by CO2 etc
- 13. Normal 300-500 mmHg Abnormal <300 mmHg Severehypoxemia <200 mmHg •
- 14. • • "A" = alveolaroxygenation "a" = arterial oxygenation
- 15. • • • • • OI = [meanairway pressure x FiO2 ÷ PaO2] x 100
- 16. • Hypoventilation V/Q mismatch Right-to-left shunt Diffusionimpairment Reduced inspired O2 tension
- 17.
- 18. Hypoxemia due topure hypoventilation (A-a gradient – not elevated ) 1 It readily corrects with a small increase in the fraction of inspired oxygen (FiO2) 2 PaCO2 is elevated An exception exists when the hypoventilation is prolonged because atelectasis can occur, which will increase the A-a gradient.
- 19. HYPOVENTILATION 3 Impaired neural conduction ALS, GBS, highcervical spine injury, phrenic N paralysis, or aminoglycoside blockade 2 Obesity hypoventilation 1 CNS depression drug overdose, structural CNS lesions, or ischemic CNS lesions that impact the respiratory center 4Muscular weakness myasthenia gravis, idiopathic diaphragmatic paralysis, polymyositis, muscular dystrophy, or severe hypothyroidism 5 Poor chest wall elasticitya flail chest or kyphoscoliosis
- 20. • • greater inthe bases • • V/Q ratio is higher in the apices • A low alveolar oxygen content; high CO2 content A low CO2 content; high oxygen content V/Q = 3 V/Q = 0.6
- 21. • • • A low alveolar oxygencontent; high CO2 content A low CO2 content; high oxygen content V/Q = 3 V/Q = 0.6 COPD Pulm Vasc d/s ILD In the diseased lung
- 22. • when the alveoliare bypassed Anatomic shunts when non-ventilated alveoli are perfused Physiologic shunts Intracardiac shunts Pulm AV malformation Hepatopulm Syndrome Atelectasis D/s with alveolar filling •Pneumonia •ARDS
- 23. • • • CaO2 and CvO2are calculated from arterial and mixed venous blood gas measurements, respectively. CcO2 is estimated from the PAO2. shunt fraction end-capillary oxygen content arterial oxygen content mixed venous oxygen content
- 24.
- 25. Alveolar Partialpressure Time in capillary(sec) 0.25 0.50 0.75 Start of capillary End of capillary CO N2O O2 (normal) O2 (abnormal) Diffusion limited Perfusion limited
- 26. The diffusion reservesof the normal lung are enormous.
- 27. The diffusion processis challenged by: Exercise Alveolar hypoxia Blood-gas barrier thickening
- 28. Pulmonary capillaries dilate Increases the surfacearea available for gas exchange Perfuse additional regions of lung PAO2 also increases Increased the oxygen gradient from the alveolus to the artery Full oxygenation is sustained Insufficient time for oxygenation Parenchymal destruction Impossible to recruit additional surface area for gas exchange Measurable hypoxemia
- 29. inspired oxygen tension fractionof inspired oxygen (0.21 at room air) atmospheric pressure (760 mmHg at sea level) partial pressure of water (47 mmHg at 37 degrees C)
- 30. • • • A reduced PiO2is most commonly associated with high altitude.
- 31.
Editor's Notes
- #3 The process of taking oxygen from the inspired air and using it to sustain aerobic cellular metabolism throughout the body can be conceptualized as having three steps:
- #5 There are numerous ways to measure whether oxygenation is impaired and at risk of being insufficient to meet the metabolic requirements of the peripheral tissues.
- #7 When administering oxygen a resting saturation at sea level should typically
- #8 A small amount of the oxygen that diffuses from the alveolus to the pulmonary capillary dissolves into the plasma.
- #9 A threshold below which tissue hypoxia predictably occurs has not been identified.
- #10 It is the difference between the amount of the oxygen in the alveoli (ie, the alveolar oxygen tension [PAO2]) and the amount of oxygen dissolved in the plasma (PaO2).
- #11 FiO2 - fraction of inspired oxygen (0.21 at room air), Patm is the atmospheric pressure (760 mmHg at sea level), PH2O is the partial pressure of water (47 mmHg at 37ºC), PaCO2 is the arterial carbon dioxide tension, and R is the respiratory quotient. The respiratory quotient is approximately 0.8 The respiratory quotient is approximately 0.8 at steady state, but varies according to the relative utilization of carbohydrate, protein, and fat. The A-a gradient calculated using this alveolar gas equation may deviate from the true gradient by up to 10 mmHg. This reflects the equation's simplification from the more rigorous full calculation and the imprecision of several independent variables (eg, FiO2 and R).
- #12 A-a equation - less accurate at higher FiO2
- #13 High A-a gradients are associated with oxygen transfer/gas exchange problems. Alveolar membrane diseases, Interstitial diseases, or V/Q mismatch Hypoxemia / normal A-a gradient: hypoventilation with displacement of alveolar O2 by CO2 or other substance. The equation for expected A-a gradient assumes the patient is breathing room air; therefore, it is less accurate at higher percentages of inspired oxygen.
- #15 Its lower limit of normal is 0.77 to 0.82 It is most reliable when the FiO2 is less than 0.55
- #17 Hypoxemia does not necessarily indicate tissue hypoxia.
- #18 The lung alveolus is a space in which gas makes up 100 percent of the contents. This means that once the partial pressure of one gas rises, the other must decrease. Both arterial (PaCO2) and alveolar (PACO2) carbon dioxide tension increase during hypoventilation, which causes the alveolar oxygen tension (PAO2) to decrease. As a result, diffusion of oxygen from the alveolus to the pulmonary capillary declines with a net effect of hypoxemia and hypercapnia. Because the respiratory quotient (Defined as CO2 eliminated/O2 consumed) is assumed to be 0.8, hypoventilation affects PaCO2 more than O2.
- #19 Hypoxemia due to pure hypoventilation (ie, in the absence of an elevated A-a gradient) can be identified by two characteristics. First, it readily corrects with a small increase in the fraction of inspired oxygen (FiO2). Second, the paCO2 is elevated. An exception exists when the hypoventilation is prolonged because atelectasis can occur, which will increase the A-a gradient
- #21 It causes the composition of alveolar gas to vary among lung regions: ●Lung regions with low ventilation compared to perfusion will have a low alveolar oxygen content and high CO2content ●Lung regions with high ventilation compared to perfusion will have a low CO2 content and high oxygen content
- #22 Common causes of hypoxemia due to V/Q mismatch include obstructive lung diseases, pulmonary vascular diseases, and interstitial diseases.
- #27 the PO2 in a red blood cell entering the capillary is normally about 40 mm Hg. Across the blood-gas barrier, only 0.3 µm away, is the alveolar PO2 of 100 mm Hg. Oxygen floods down this large pressure gradient, and the PO2 in the red cell rapidly rises; indeed, as we have seen, it very nearly reaches the PO2 of alveolar gas by the time the red cell is only one-third of its way along the capillary. Thus, under normal circumstances, the difference in PO2 between alveolar gas and end-capillary blood is immeasurably small—a mere fraction of a mm Hg. In other words, the diffusion reserves of the normal lung are enormous. With severe exercise, the pulmonary blood flow is greatly increased, and the time normally spent by the red cell in the capillary, about 0.75 second, may be reduced to as little as one-third of this. Therefore, the time available for oxygenation is less, but in normal subjects breathing air there is generally still no measurable fall in end-capillary PO2. However, if the blood-gas barrier is markedly thickened by disease so that oxygen diffusion is impeded, the rate of rise of PO2 in the red blood cells is correspondingly slow, and the PO2 may not reach that of alveolar gas before the time available for oxygenation in the capillary has run out. In this case, a measurable difference between alveolar gas and end-capillary blood for PO2 may occur. Another way of stressing the diffusion properties of the lung is to lower the alveolar PO2 (Figure 3-3B). Suppose that this has been reduced to 50 mm Hg, by the subject either going to high altitude or inhaling a low O2 mixture. Now, although the PO2 in the red cell at the start of the capillary may only be about 20 mm Hg, the partial pressure difference responsible for driving the O2 across the blood-gas barrier has been reduced from 60 mm Hg (Figure 3-3A) to only 30 mm Hg. O2 therefore moves across more slowly. In addition, the rate of rise of PO2 for a given increase in O2 concentration in the blood is less than it was because of the steep slope of the O2 dissociation curve when the PO2 is low (see Chapter 6). For both of these reasons, therefore, the rise in PO2 along the capillary is relatively slow, and failure to reach the alveolar PO2 is more likely. Thus, severe exercise at very high altitude is one of the few situations in which diffusion impairment of O2 transfer in normal subjects can be convincingly demonstrated. By the same token, patients with a thickened blood-gas barrier will be most likely to show evidence of diffusion impairment if they breathe a low oxygen mixture, especially if they exercise as well.