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                  64    PA R T  I / Anatomy and Physiology
                  maximum amount of oxygen carried by 1 gram of Hgb. This ex-  Oxygen consumption is affected by several factors. Blood flow de-
                  pression is depicted in the following equation:     pends on the cardiac output and on the degree of constriction of
                                                                      the vascular bed in the tissue (vasoregulatory mechanisms). Low
                          (Hgb   1.36   Sa O2 ) 
 (0.0031   Pa O2 )
                                 97%             3%                   Hgb decreases the amount of available oxygen to be delivered to
                                                                      the tissues. Reduced Pa O2 can affect the driving force needed to
                                                     equal to 100 mm
                                                                      load the oxygen molecule on the Hgb. Decreased Sa O2 affects the
                  Assuming a normal Hgb of 15 g, arterial Pa O 2
                  Hg, and 98% saturation, the arterial oxygen content (Ca O2 ) is 20
                                                                      affinity between oxygen and Hgb, enhancing the release of oxygen
                  mL/dL. The equation can also be used to determine venous oxy-
                                                                      to the tissues. The metabolic rate of the tissues also affects the
                                ). Assuming no change in the Hgb and a ve-
                                                                      affinity of oxygen to be released.
                  gen content (Cv O 2
                  nous Pa O2 of 40 mm Hg and 75% saturation, the venous oxygen
                  content is 15 mL/dL.                                Oxygen Extraction Ratio
                                                                      The percentage of oxygen extracted by the tissues is a useful indi-
                  Measurement of Oxygen Delivery                      cator of the balance between oxygen delivery and consumption.
                                                          ˙
                                            ˙
                                                          Q
                                                          Q
                  Measurement of oxygen delivery (DO 2 ) or transport (QO 2 ) is cal-  Oxygen extraction represents the difference between arterial and
                  culated by multiplying total arterial oxygen content by cardiac  venous oxygen contents (normal 5 mL/dL or 25%) and is known
                  output (CO):                                        as the C(a–v) O2 difference or oxygen extraction ratio (O 2 ER). This
                                 ˙                                    ratio increases in pathological conditions characterized by an im-
                                DO 2   CO   Ca O 2    10
                                                                      balance between oxygen delivery and VO 2 . O 2 ER is increased by
                                                               )      factors such as decreased cardiac output, increased oxygen con-
                     where Ca O 2    (Hgb 1.36  Sa O 2 ) 
 (0.0031   Pa O 2
                                               13.6                   sumption (e.g., shivering), anemia, and decreased arterial oxygena-
                                CO Hgb  Sa O 2
                                                                      tion. O 2 ER is decreased in conditions where VO 2 is relatively low
                                                         of 20 mL/dL,
                  In patients with cardiac output of 5 L/min and a Ca O 2  in proportion to oxygen delivery, such as in sepsis, hypothermia,
                                    ˙
                  arterial oxygen delivery (DO 2 ) is 1,000 mL of oxygen/min or on av-  high-flow states, peripheral shunting, or cytopathic hypoxia. 180,187
                                      2
                  erage 500 to 650 ml/min/m . Critical oxygen delivery, which reflects
                  the point where oxygen delivery fails to satisfy metabolic needs for
                                                       ˙
                  oxygen has not been definitively identified. Critical DO 2 has been es-  R EFERENCES
                  timated to be less than 7 ml/kg/min in awake, healthy young adults  1. Wiedeman, M. (1963). Dimensions of blood vessels from distributing
                                2
                  and 330 ml/min/m in anesthetized older adults. 189–191  artery to collecting vein. Circulation Research, 12, 375–378.
                     Delivery of oxygen to support aerobic metabolism can be lim-  2. Rothe, C. (1983). Venous system: Physiology of the capacitance vessels.
                                                                          In J. Shepherd & F. Abboud (Eds.), Handbook of physiology. The cardio-
                  ited anywhere along the route from the environment through the
                                                                          vascular system. Peripheral circulation and organ blood flow (pp. 397–452).
                  alveolar–pulmonary interface, the systemic circulation, and  Bethesda, MD: American Physiological Society.
                  the capillary–tissue junction to the mitochondria. Hypoxia is the  3. Rhodin, J. (1980). Architecture of the vessel wall. In D. Bohr, A. Somlyo,
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                                                                        4. Rhodin, J. (1981). Anatomy of the microcirculation. In R. Effros, H.
                  caused by decreased Hgb; (3) ischemic (stagnant) hypoxia, caused
                                                                          Schmid-Schonbein & J. Ditzel (Eds.), Microcirculation (pp. 11–17).
                  by a lack of blood flow to the tissue; and (4) histotoxic (cytopathic)  New York: Academic Press.
                  hypoxia, normal oxygen delivery; however, the cell is unable to  5. Dalton, S. R., Fillman, E. P., Ferringer, T., et al. (2006). Smooth muscle
                  process the oxygen and produce ATP.                     pattern is more reliable than the presence or absence of an internal elas-
                                                                          tic lamina in distinguishing an artery from a vein. Journal of Cutaneous
                                                                          Pathology, 33, 216–219.
                  Oxygen Consumption                                    6. O’Rourke, M. F. (2007). Arterial aging: Pathophysiological principles.
                                    ˙
                  Oxygen consumption (VO 2 ) is the body’s demand for oxygen and  Vascular Medicine, 12, 329–341.
                  is defined as the amount of oxygen consumed at the tissue level  7.Mulvany, M., & Aalkjeær, C. (1990). Structure and function of small ar-
                  per minute. Oxygen consumption can be calculated by determin-  teries. Physiology in Review, 70, 922–961.
                                                                        8. Mulvany, M. (1996). The Seventh Heymans Memorial Lecture Ghent,
                  ing the difference between the quantity of oxygen carried by the
                                                                          February 18, 1995. Physiological aspects of small arteries. Archives of
                  arterial system to the tissues (Ca O2 ) and the quantity remaining in  International Pharmacodynamic Therapeutics, 331, 1–31.
                  the blood returning in the venous system to the lungs (Cv O2 )  180 :  9. Faber, J. (1988). In situ analysis of alpha-adrenoreceptors on arteriolar
                                                                          and venular smooth muscle in rat skeletal muscle microcirculation.
                       ˙
                       VO 2   (CO   Ca O2   10)   (CO   Cv O2   10)       Circulation Research, 62, 37–50.
                                   ˙                                   10. Rizzoni, D., Porteri, E., Boari, G. E., et al. (2003). Prognostic significance
                                  VO 2   Ca O2   Cv O2
                                                                          of small-artery structure in hypertension. Circulation, 108, 2230–2235.
                  By combining the factors, the preceding can be simplified to the  11. De Ciuceis, C., Porteri, E., Rizzoni, D., et al. (2007). Structural alter-
                  following equation:                                     ations of subcutaneous small-resistance arteries may predict major car-
                                                                          diovascular events in patients with hypertension. American Journal of
                          ˙
                         VO 2   CO   Hgb   13.6   (Sa O2   Sv O2 )        Hypertension, 20, 846–852.
                                                        v v
                                                                       12. Mulvany, M. J. (2007). Small artery structure: Time to take note? American
                                                                ˙
                  This equation is a restatement of the Fick equation, placing VO 2  Journal of Hypertension, 20, 853–854.
                  on the left instead of cardiac output. This formula identifies all  13. Renkin, E. (1989). Microcirculation and exchange. In H. Patton, A.
                  components of oxygen supply and demand. In a patient with nor-  Fuches, B. Hille, et al. (Eds.), Textbook of physiology (pp. 860–878).
                                                     ˙
                  mal values in a relatively steady state, normal VO 2 is on average  Philadelphia: WB Saunders.
                                                                       14. Renkin, E. (1984). Control of microcirculation and blood-tissue ex-
                  between 200 and 250 mL/min (or estimates of 3.5 mL/kg), as  change. In E. Renkin & C. Michel (Eds.), Handbook of physiology (pp.
                  shown in the following equation:                        627–687). Bethesda, MD: American Physiological Society.
                        ˙
                        VO 2   5 L/min   15 g/dL   13.6 (0.98   0.75)  15. Sarelius, I. H., Cohen, K. D., & Murrant, C. L. (2000). Role for capil-
                                                                          laries in coupling blood flow with metabolism. Clinical Experiments in
                                   ˙
                                   VO 2   234 mL/min                      Pharmacology and Physiology, 27, 826–829.
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