Cardiovascular And Tissue Oxygen Transport

The cardiovascular system is responsible for transporting O2 to metabolizing tissues after it has diffused into pulmonary capillary blood. The heart pumps 02-rich arterial blood to the tissues, where O2 leaves the systemic capillaries and moves to the mitochondria through tissue gas exchange. The heart also pumps O2-poor venous blood back to the lungs, where it is reoxygenated. The magnitude of the Po2 decrease between arterial and venous blood (see Fig. 1) depends on both the cardiovascular O2 supply and O2 demand in the tissues.

Cardiovascular Oxygen Transport

O2 supply, or delivery, to tissues can be defined as the product of cardiac output and arterial O2 concentration (Q Cao2). The tissues will extract enough O2 to meet their metabolic demands, as long as O2 supply is sufficient. Hence, O2 supply and demand determine venous O2 levels. These factors are related by the Fick principle (Chapter 18), which describes O2 transport by the cardiovascular system as follows:

V02 = Q(Cao2 - CV02), where Vo2 is 02 consumption, Q is cardiac output, and the last term is the arterial-venous 02 concentration difference. This equation can be rearranged and used to calculate cardiac output from measurements of Vo2 and blood 02 concentrations.

The Fick principle can be used to predict the arterial-venous O2 concentration difference from normal resting values for 02 consumption (Vo2 = 300 mL/min) and cardiac output (Q = 6 L/min): (300 mL of 02/min)/(6000 mL of blood/min) = 5 mL 02/dL blood. If the normal value for Cao2 = 20 mL of 02/dL

Erythropoietic Ventilatory

Erythropoietic Ventilatory

Pq2 Blood flow

FIGURE 5 Left-blood-02 equilibrium curve showing arterial (a) and mixed-venous (V) points. Right-graphical representation of the Fick principle for cardiovascular 02 transport. Horizontal axis is blood flow normalized to body mass; vertical axis is 02 concentration from the left panel; shaded area is 02 consumption. "Reserves," which can increase Vo2, are described in the text. (After Woodson, Basics of Respiratory Disease, 5:1, 1977.)

Pq2 Blood flow

FIGURE 5 Left-blood-02 equilibrium curve showing arterial (a) and mixed-venous (V) points. Right-graphical representation of the Fick principle for cardiovascular 02 transport. Horizontal axis is blood flow normalized to body mass; vertical axis is 02 concentration from the left panel; shaded area is 02 consumption. "Reserves," which can increase Vo2, are described in the text. (After Woodson, Basics of Respiratory Disease, 5:1, 1977.)

of blood, then CVo2 =15 mL/dL. Notice that venous 02 level is determined by (1) the ratio of metabolism to blood flow and (2) arterial 02 concentration, which is determined by alveolar Po2 and the blood-02 equilibrium curve. The 02-blood equilibrium curve (see Chapter 20, Fig. 1) is used to convert CVo2 (15 mL/dL) to mixed-venous 02 saturation (75%) and PVo2 (40 mm Hg).

Figure 5 shows the cardiovascular Fick principle graphically, to illustrate the importance of the shape of the 02-blood equilibrium curve. In the right panel, the height of the shaded rectangle represents the arterial-venous 02 concentration difference, and its width represents cardiac output (normalized to 100 g of body mass). The area of the rectangle is the product of these two factors, and represents Vo2.

Changes in Vo2 can be achieved by increasing cardiac output (''flow reserve'') and/or increasing the arterial-venous 02 difference. The dashed lines on Fig. 5 show the consequences of increasing Vo2 by increasing venous 02 extraction (extraction reserve). Changes in PVo2, are minimized with large decreases in venous 02 concentration by the shape of the 02-blood equilibrium curve. A right shift of the 02-blood equilibrium curve can increase PVo2 for a given CVo2 (O2-dissociation reserve). Maintaining a high PVo2, is important for tissue gas exchange and the microcirculatory and tissue reserve, as discussed later. All of these reserves are important mechanisms for meeting increased 02 demands during exercise.

Increases in O2 delivery are achieved primarily through increases in cardiac output in normoxic conditions. Increasing alveolar and arterial PO2 is not effective at increasing CaO2 in normoxic conditions because the slope of the O2-blood equilibrium curve is flat at normal Pao2 values (ventilatory reserve; Fig. 5). However, changes in PaO2 are much more effective at changing O2 delivery when PO2 is low, for example, at altitude, when exchange occurs on a steeper part of the O2-blood equilibrium curve. Changes in hematocrit and hemoglobin concentration, which occur with chronic hypoxia (see Chapter 20), can increase O2 delivery by increasing total O2 concentration for any given PO2 (erythropoietic reserve). The erythropoietic reserve is the physiologic basis for the questionable practice of''blood doping,'' which uses blood transfusions or artificial erythropoietin in attempts to increase maximal O2 consumption and athletic performance.

Tissue Gas Exchange

O2 moves out of systemic capillaries to the mitochondria in cells by diffusion. Therefore, O2 transport in tissues is described by Fick's first law of diffusion, similar to diffusion across the blood-gas barrier in the lung:

v-o2 = APo2 • Dto2, where APo2 is the average Po2 gradient between capillary blood and the mitochondria, and DtO2 is a tissue-diffusing capacity for O2. Interestingly, anatomic estimates of DtO2 for the whole body are similar to anatomic estimates of DmO2 in the lung.

The main difference between O2 diffusion in tissue and in the lung is that diffusion pathways are much longer in tissue. Tissue capillaries may be 50 mm apart, so the distance from a capillary surface to mitochondria can be 50 times longer than the thickness of the blood-gas barrier (<0.5 mm). Long diffusion distances can lead to significant Po2 gradients in tissues. Also, the Po2 gradient varies along the length of a capillary as O2 leaves the blood, and capillary PO2 decreases from arterial to venous levels. A mathematical model called the Krogh cylinder can be used to predict PO2 profiles in metabolizing tissue. This model predicts that PO2 in cells farthest away from a capillary, or at the venous end of the capillary, may be zero when O2 demand is increased. However, mitochondria function normally until PO2 decreases below a few mm Hg (see Chapter 18, Fig. 1), so metabolism will continue under all but these most extreme conditions.

During increased O2 demand (e.g., exercise in skeletal muscle, absorption in the gut, nervous activity in the brain), additional capillaries may be recruited

(Chapter 17). This helps maintain adequate O2 supply by decreasing diffusion distances. Factors increasing, or maintaining, PVo2 also help tissue O2 diffusion by enhancing the PO2 gradient. These factors include the steep shape of the O2-blood equilibrium curve in the venous range and right shifts of the curve by temperature, Pco2, and pH changes, for example, in exercising muscle. PVo2 is sometimes used as an index of tissue O2 exchange because it represents the minimum pressure head driving O2 diffusion in the body.

Myoglobin may facilitate O2 diffusion in muscle by shuttling O2 to sites far away from a capillary. Recent measurements show that PO2 in skeletal muscle is much more uniform than predicted by the Krogh cylinder model and that myoglobin may shuttle O2 to the venous end. The implications of this finding for differences in O2 transport between muscle (e.g., during myocardial ischemia) and brain (e.g., during a stroke) remain to be determined.

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